TEST BANK for Psychopharmacology: Drugs, the Brain, and Behavior 4th Edition by Jerry Meyer | All Ch

Test Bank to accompany

Psychopharmacology, Fourth Edition Meyer • Quenzer

Chapter 1: Principles of Pharmacology Multiple Choice 1. refer(s) to specific molecular changes that occur when a drug binds to a particular target site or receptor, while are the resulting widespread alterations in function. a. Drug action; therapeutic effects b. Side effects; drug effects c. Therapeutic effects; side effects d. Drug action; drug effects Answer: d Textbook Reference: Pharmacology: The Science of Drug Action 2. After drug administration has occurred, the amount of drug in the blood that is free to bind at specific target sites is referred to as a. the therapeutic dose. b. first-pass effects. c. bioavailability. d. ED 50 .

Answer: c Textbook Reference: Pharmacokinetic Factors Determining Drug Action 3. The specific molecular changes that occur when a drug binds to a particular target site or receptor are referred to as a. drug effects. b. drug action. c. side effects. d. placebo effects.

Answer: b Textbook Reference: Pharmacology: The Science of Drug Action 4. Which of the following is not a possible explanation for placebo effects? a. Pavlovian conditioning b. Genetic variation c. Drug competition d. Expectation of outcome Answer: c Textbook Reference: Pharmacology: The Science of Drug Action

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5. The administration of oxytocin has been proposed as a treatment for autism. a. intravenous b. oral c. intranasal d. intracerebral Answer: c Textbook Reference: Pharmacokinetic Factors Determining Drug Action 6. Which factor does not affect the pharmacokinetics of a drug? a. Route of administration b. Lipid solubility c. Depot binding d. Drug action Answer: d Textbook Reference: Pharmacokinetic Factors Determining Drug Action 7. First-pass metabolism occurs when drugs are taken a. orally. b. intravenously. c. subcutaneously. d. nasally.

Answer: a Textbook Reference: Pharmacokinetic Factors Determining Drug Action 8. The area postrema is one area in the brain where the is not complete. a. cerebrospinal fluid b. blood–brain barrier c. choroid plexus d. phospholipid membrane Answer: b Textbook Reference: Pharmacokinetic Factors Determining Drug Action 9. First-pass metabolism occurs with orally administered drugs because a. their absorption is slowed by food. b. drugs absorbed into the bloodstream from the stomach go to the liver on the way to general circulation. c. drugs must first survive the acidic environment of the stomach. d. salivary enzymes in the mouth begin the process of metabolism.

Answer: b Textbook Reference: Pharmacokinetic Factors Determining Drug Action 10. Toxic substances in the blood trigger a vomiting response by activating the a. blood–brain barrier. b. choroid plexus. c. area postrema. d. median eminence.

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Answer: c Textbook Reference: Pharmacokinetic Factors Determining Drug Action 11. Drugs administered _ have the most rapid onset of action. a. subcutaneously b. intramuscularly c. orally d. intravenously Answer: d Textbook Reference: Pharmacokinetic Factors Determining Drug Action 12. Ionization of a drug depends on the of the solution and the drug. a. pH; pK a b. pK a; pH c. concentration; lipid solubility d. pH; concentration Answer: a Textbook Reference: Pharmacokinetic Factors Determining Drug Action

of the

13. The absorption of a drug depends on all of the following except a. lipid solubility. b. ionization. c. body temperature. d. the concentration of the drug.

Answer: c Textbook Reference: Pharmacokinetic Factors Determining Drug Action 14. Drugs that are should be avoided by women of childbearing age. a. teratogenic b. able to cross the placental barrier c. psychoactive d. highly lipid-soluble Answer: a Textbook Reference: Pharmacokinetic Factors Determining Drug Action 15. Agents that induce developmental abnormalities in a fetus are known as a. psychoactive drugs. b. illicit drugs. c. teratogens. d. placental drugs.

Answer: c Textbook Reference: Pharmacokinetic Factors Determining Drug Action 16. Depot binding is said to occur when drugs a. bind to their target sites.

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b. bind to inactive sites. c. compete for binding sites. d. are excreted before binding.

Answer: b Textbook Reference: Pharmacokinetic Factors Determining Drug Action 17. Which statement about depot binding is false? a. It reduces the concentration of drug at its site of action. b. It may delay the onset of drug action. c. It may prolong drug action by disrupting normal metabolism. d. It increases the concentration of drug at its site of action by releasing large quantities at once.

Answer: d Textbook Reference: Pharmacokinetic Factors Determining Drug Action 18. Drug metabolism mostly occurs in the and usually makes a drug more soluble. a. kidneys; fat b. liver; fat c. liver; water d. kidneys; water Answer: c Textbook Reference: Pharmacokinetic Factors Determining Drug Action 19. Which statement about drug clearance by first-order kinetics is false? a. Molecules of a drug are cleared at a constant rate regardless of drug concentration. b. Molecules of a drug are cleared at an exponential rate. c. A constant fraction of the free drug in the blood is removed in each time interval. d. Clearance of most drugs occurs in this manner.

Answer: a Textbook Reference: Pharmacokinetic Factors Determining Drug Action 20. Ethyl alcohol (ethanol) is an example of a drug that is eliminated a. by first-order kinetics. b. by zero-order kinetics. c. by second-order kinetics. d. at the point that six half-lives have passed.

Answer: b Textbook Reference: Pharmacokinetic Factors Determining Drug Action 21. Biotransformation of drugs in the liver often occurs in two stages; phase I changes are and include . a. nonsynthetic; conjugation b. synthetic; conjugation c. nonsynthetic; oxidation d. synthetic; oxidation

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Answer: c Textbook Reference: Pharmacokinetic Factors Determining Drug Action 22. Biotransformation of drugs can result in the formation of , which enter the circulation and cause . a. inactive metabolites; sensitization b. active metabolites; prolonged drug action c. active metabolites; tolerance d. enzymes; tolerance Answer: b Textbook Reference: Pharmacokinetic Factors Determining Drug Action 23. Which statement about water-soluble metabolites formed in the liver is false? a. They may return to the circulation and act on target tissues. b. They may be filtered out by the kidneys. c. They may be excreted into bile. d. They may be eliminated with the feces.

Answer: a Textbook Reference: Pharmacokinetic Factors Determining Drug Action 24. Which statement about microsomal enzymes in the liver is false? a. They are highly specific and act only on certain compounds. b. They are located on the smooth endoplasmic reticulum. c. The cytochrome P450 family is one of the most important. d. They can metabolize toxins and environmental pollutants as well as drugs.

Answer: a Textbook Reference: Pharmacokinetic Factors Determining Drug Action 25. Repeated use of many psychoactive drugs can cause , which can speed up the rate of biotransformation of these drugs as well as others. a. drug competition b. enzyme inhibition c. enzyme induction d. tolerance Answer: c Textbook Reference: Pharmacokinetic Factors Determining Drug Action 26. Due to , antidepressants known as monoamine oxidase inhibitors (MAOIs) can cause cardiac arrhythmias and high blood pressure in patients that consume foods high in tyramine. a. sensitization b. tolerance c. drug competition d. enzyme inhibition Answer: d Textbook Reference: Pharmacokinetic Factors Determining Drug Action

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27. While drugs can be excreted from the body by several routes, the most important route of elimination is through the a. breath. b. sweat. c. feces. d. urine.

Answer: d Textbook Reference: Pharmacokinetic Factors Determining Drug Action 28. The liver and kidneys work together to _ and drugs, respectively. a. metabolize; excrete b. excrete; metabolize c. bind; metabolize d. absorb; excrete Answer: a Textbook Reference: Pharmacokinetic Factors Determining Drug Action 29. For drugs that have a narrow therapeutic window or potentially serious side effects, therapeutic drug monitoring uses to determine the optimum dosage for a new patient. a. body temperature b. urine testing c. brain scans d. blood sampling Answer: d Textbook Reference: Therapeutic Drug Monitoring 30. While pharmacokinetics describes how the body deals with drugs, how drug molecules interact with their targets. a. drug effect b. pharmacodynamics c. antagonist action d. agonist action Answer: b Textbook Reference: Pharmacodynamics: Drug–Receptor Interactions

describes

31. In order for a drug to have an effect, it must first bind to a a. ligand. b. depot site. c. receptor. d. neurotransmitter.

Answer: c Textbook Reference: Pharmacodynamics: Drug–Receptor Interactions 32. Most drugs and neurotransmitters act upon

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a. intracellular receptors. b. membrane-bound receptors. c. protein synthesis. d. second messengers.

Answer: b Textbook Reference: Pharmacodynamics: Drug–Receptor Interactions 33. While most receptors are membrane-bound on the cell surface, many receptors are intracellular. a. drug; neurotransmitter b. hormone; drug c. neurotransmitter; hormone d. agonist; antagonist Answer: c Textbook Reference: Pharmacodynamics: Drug–Receptor Interactions 34. Ligands that have no effect on a receptor after binding are called a. antagonists. b. agonists. c. neurotransmitters. d. null ligands.

Answer: a Textbook Reference: Pharmacodynamics: Drug–Receptor Interactions 35. Both agonists and antagonists have but only agonists have appreciable . a. interactions; affinity b. affinity; bioavailability c. efficacy; affinity d. affinity; efficacy Answer: d Textbook Reference: Pharmacodynamics: Drug–Receptor Interactions 36. A dose–response curve shows that noncompetitive antagonists alter both the and the of the agonist, while competitive antagonists alter only the a. potency; efficacy; potency b. bioavailability; metabolism; bioavailability c. efficacy; potency; efficacy d. depot binding; metabolism; metabolism Answer: a Textbook Reference: Pharmacodynamics: Drug–Receptor Interactions

.

37. In the dose–response curve, a decrease in potency is indicated by a shift a. to the left. b. to the right. c. upward.

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d. downward.

Answer: b Textbook Reference: Pharmacodynamics: Drug–Receptor Interactions 38. Which of the following describes the interaction of two drugs when the combined drug effects are greater than would be predicted from that combination? a. Addictive effects b. Physiological antagonism c. Potentiation d. Tolerance Answer: c Textbook Reference: Pharmacodynamics: Drug–Receptor Interactions 39. After chronic use, the need to administer more of a drug to achieve the same drug effect is known as a. sensitization. b. antagonism. c. potentiation. d. tolerance.

Answer: d Textbook Reference: Biobehavioral Effects of Chronic Drug Use 40. Which factor does not cause tolerance? a. Conditioning b. Increased activity of liver enzymes c. Down-regulation of receptors d. Decreased kidney function Answer: d Textbook Reference: Biobehavioral Effects of Chronic Drug Use 41. Sensitization is most often seen with which class of drugs? a. Barbiturates b. Psychomotor stimulants c. Opiates d. Hallucinogens Answer: b Textbook Reference: Biobehavioral Effects of Chronic Drug Use 42. tolerance occurs as a result of cellular adaptation to the presence of a specific drug. a. Cross b. Drug disposition c. Pharmacodynamic d. Behavioral Answer: c Textbook Reference: Biobehavioral Effects of Chronic Drug Use

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43. Which of the following is not a goal of pharmacogenetics? a. Assessing addiction potential b. Selecting the best drug for a given individual c. Predicting therapeutic outcome d. Minimizing serious toxic reactions Answer: a Textbook Reference: Pharmacogenetics and Personalized Medicine in Psychiatry

Short Answer/Essay 44. Write a coherent and informative paragraph using the following terms: nonspecific drug effects, double-blind experiment, placebo, subject expectation.

Answer: In contrast to specific drug effects that are dependent on the chemical activity of a drug–receptor interaction, nonspecific drug effects are determined by characteristics of the individual such as present mood or drug-taking experience. Placebo effects are an example of nonspecific effects because placebos have no chemical activity but depend on the expectations of the individual. Placebos are an important control in double-blind experiments because neither the patient nor the observer knows if the patient has received the active drug or placebo in order to avoid expectation of results or prejudice.

Textbook Reference: Pharmacology: The Science of Drug Action 45. List the factors that can influence biotransformation, and briefly explain how they can lead to individual differences in drug response.

Answer: Biotransformation can be influenced by enzyme induction, enzyme inhibition, drug competition, and individual differences in age, gender, and genetics. The increase in metabolizing enzymes (induction) increases the rate of biotransformation, causing tolerance. Inhibition of an enzyme by a drug increases the blood level of other drugs metabolized by that enzyme, causing toxicity. When two drugs compete for the limited number of enzyme molecules, higher blood levels of one or both may occur. Both young and older individuals have reduced metabolic capacity; men and women vary in enzyme activity, and genetic polymorphisms alter the rate of biotransformation.

Textbook Reference: Pharmacokinetic Factors Determining Drug Action 46. Explain why absorption of aspirin is slower from the intestine than from the stomach.

Answer: Because aspirin is a weak acid, it will remain in a non-ionized (lipid soluble) form in the acidic stomach and hence it will pass through the cell walls of the stomach to the blood. In the intestine, where the pH is more alkaline, the aspirin molecules will ionize to a greater extent, which reduce their movement through the cell walls to the blood.

Textbook Reference: Pharmacokinetic Factors Determining Drug Action 47. List and briefly describe the five major factors that determine the pharmacokinetics of drug action.

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Answer: Routes of administration determine how quickly and how completely the drug is absorbed into the blood. Absorption of the drug through cell membranes and into the blood precedes the distribution of the drug to all the cells in the body. Binding of the drug may occur at active target sites, to inert depots such as plasma proteins, or stored in bone or fat. Biotransformation influences the intensity and duration of drug effects because the amount of drug in the body at any one time is dependent on the dynamic balance between absorption and inactivation. Excretion of the drug with urine or feces eliminates it from the body.

Textbook Reference: Pharmacokinetic Factors Determining Drug Action 48. Define the therapeutic index and describe how it is calculated and why it is important.

Answer: The therapeutic index is a measure of drug safety and it is calculated by comparing the dose of a drug that produces a particular drug-induced toxic effect in 50% of a given population with the dose of the drug that produces a particular therapeutic effect. (TI = TD 50 / ED 50 ) When the TD 50 and ED 50 are very similar the TI is low and the probability of a toxic effect is great. When the TD 50 is large and the ED 50 is low, many patients will benefit from the drug and few will experience the toxic effect.

Textbook Reference: Pharmacodynamics: Drug–Receptor Interactions 49. Draw the dose–response curves for two drugs with the same efficacy, given that drug A is ten times as potent as drug B. Answer: See sample figure below.

Textbook Reference: Pharmacodynamics: Drug–Receptor Interactions 50. Compare and contrast competitive and noncompetitive antagonists.

Answer: Both types of antagonists reduce the effects of agonists, but by different means.

Competitive antagonists compete with agonists binding to receptors, but can be displaced by excess agonist. Hence, although the potency of an agonist is reduced and its dose– response curve is shifted to the right, its efficacy is not changed. In contrast,

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noncompetitive antagonists reduce the effects of agonists in ways other than receptor competition, such as disturbing the receptor’s cell membrane environment. In these cases the dose–response curve is distorted rather than shifted and the same maximum (efficacy) is not achieved.

Textbook Reference: Pharmacodynamics: Drug–Receptor Interactions 51. Define and explain receptor up-regulation and down-regulation.

Answer: Receptor up-regulation is an increase in receptor number that represents a compensatory change in the cell after prolonged absence of receptor agonists. Receptor down-regulation is a decrease in receptor number and reflects a compensatory change after chronic activation of the receptor. These changes are responsible for pharmacodynamic tolerance and also explain the rebound withdrawal syndrome that is characteristic of physical dependence.

Textbook Reference: Biobehavioral Effects of Chronic Drug Use 52. Describe briefly the four types of tolerance.

Answer: Acute tolerance occurs when a individual experiences greater effects of a drug as her blood level rises than when her blood level has fallen to the same point during the same episode. Metabolic tolerance occurs when repeated use of a drug increases its own rate of metabolism. Pharmacodynamic tolerance occurs when compensatory cellular adjustments occur in response to the prolonged presence of the drug. Behavioral tolerance is dependent on several types of learning (classical conditioning and operant conditioning) and the environment in which the drug is administered.

Textbook Reference: Biobehavioral Effects of Chronic Drug Use 53. What is state-dependent learning? Why does it occur?

Answer: State-dependent learning refers to the concept that tasks learned under the influence of a psychoactive drug will subsequently be performed better in the drugged state than in the nondrugged state. Likewise, tasks learned in the nondrugged state will be performed better in the nondrugged state than in the drugged state. This occurs because drug-ind uced internal cues become part of the environmental ―set‖ and when any aspect of the environment, such as the experimental apparatus, changes, performance deteriorates.

Textbook Reference: Biobehavioral Effects of Chronic Drug Use 54. Explain how pharmacogenetic approaches could lead to better pharmacological treatment.

Answer: Pharmacogenetics investigates the genetic basis for variability in drug response among individuals. Variability can be explained by genetic differences in both pharmacokinetic and pharmacodynamic factors. However, the most studied are genetic differences in drug-metabolizing enzymes because variations in biotransformation lead to large differences in bioavailability responsible for variations in effectiveness and side effects. Knowing the inherited level of function of metabolizing enzymes could predict the correct dose for an individual to maximize benefits and avoid adverse drug effects.

Textbook Reference: Pharmacogenetics and Personalized Medicine in Psychiatry

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Test Bank to accompany

Psychopharmacology, Third Edition Meyer • Quenzer

Chapter 2: Structure and Function of the Nervous System Multiple Choice 1. Neurons rely on for protection, metabolic support, and insulation. a. mitochondria b. glial cells c. axoplasm d. dendritic spines Answer: b Textbook Reference: Cells of the Nervous System 2. Neurons responsible for converting environmental stimuli into neural signals are known as a. sensory neurons. b. interneurons. c. motor neurons. d. pyramidal cells.

Answer: a Textbook Reference: Cells of the Nervous System 3. Neurons can be categorized by all of the following except by a. which neurotransmitters they release. b. their function (e.g., sensory versus motor). c. the size of the action potentials they generate. d. their morphology.

Answer: c Textbook Reference: Cells of the Nervous System 4. The of the neuronal cell is/are found in the soma, while the found throughout the cell. a. mitochondria; dendrites b. dendrites; axon c. nucleus; mitochondria d. nucleus; dendrites Answer: c Textbook Reference: Cells of the Nervous System 5. Mitochondria are responsible for generating .

may be

for the cell in the form of

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a. energy; ATP b. energy; glucose c. cytoplasm; ATP d. cytoplasm; glucose Answer: a Textbook Reference: Cells of the Nervous System 6. Neurons exchange information primarily via a. somas. b. dendrites. c. axons. d. axon collaterals.

Answer: b Textbook Reference: Cells of the Nervous System 7. Dendritic spines serve to a. increase the surface area of the dendrite. b. insulate the axons. c. insulate the dendrites. d. protect the dendrites from degrading enzymes in the extracellular fluid.

Answer: a Textbook Reference: Cells of the Nervous System 8. The function of the axon is to transmit the terminals. a. axoplasm; soma b. action potential; axon hillock c. action potential; dendrites d. synaptic vesicles; axon hillock Answer: b Textbook Reference: Cells of the Nervous System

, generated at the

, to the

9. In a myelinated axon, action potentials are regenerated a. at the terminal buttons. b. all along the axon. c. at gaps in the myelin known as nodes of Ranvier. d. at the axon hillock.

Answer: c Textbook Reference: Cells of the Nervous System 10. Which statement about the myelin sheath is false? a. It is produced by glial cells. b. It increases the speed of signal conduction along the axon. c. It saves energy. d. It is found on all neurons.

Answer: d

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Textbook Reference: Cells of the Nervous System 11. are long strands of DNA divided into smaller portions called _ which code for specific proteins. a. Chromosomes; genes b. Genes; chromosomes c. Transcription factors; genes d. Genes; ribosomes Answer: a Textbook Reference: Cells of the Nervous System

,

12. Which statement about the process of transcription is true? a. It is driven by ribosomes. b. It occurs in the cytoplasm. c. The nucleotide sequence of DNA is replicated by mRNA. d. It results in the production of proteins.

Answer: c Textbook Reference: Cells of the Nervous System 13. Proteins, such as receptors and enzymes, are synthesized in the cytoplasm of the soma in a process called a. translation. b. regulation. c. transcription. d. transport.

Answer: a Textbook Reference: Cells of the Nervous System 14. Which of the following most accurately describes the process involved in protein synthesis? a. Transcription factors activate promoter region → translation by ribosomes → transcription by mRNA b. Transcription factors activate promoter region → transcription by mRNA → translation by ribosomes c. Translation by ribosomes → transcription factors activate promoter region → transcription by mRNA d. Transcription by mRNA → transcription factors activate promoter region → translation by ribosomes Answer: b Textbook Reference: Cells of the Nervous System 15. Epigenetic changes affect gene expression by a. blocking translation; DNA methylation b. breaking down chromatin; blocking transcription c. DNA methylation; chromatin remodeling d. remodeling transcription factors; blocking translation

and by

.

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Answer: c Textbook Reference: Cells of the Nervous System 16. Axonal transport of proteins occurs along a track formed by a. microtubules. b. neurofilaments. c. anterograde cytoskeleton. d. retrograde cytoskeleton.

Answer: a Textbook Reference: Cells of the Nervous System 17. Neuronal cell membranes are associated with all of the following proteins except a. transporters. b. ion channels. c. microtubules. d. enzymes.

Answer: c Textbook Reference: Cells of the Nervous System 18. Many ion channels are not normally open but must be gated or opened by some event.

Which of the following is not a typical means of opening ion channels? a. Binding of neurotransmitter to external binding site b. Change in voltage across the membrane c. Phosphorylation by an intracellular second messenger d. Enzymatic reactions Answer: d Textbook Reference: Cells of the Nervous System 19. With regard to glial cells, form the myelin sheath in the CNS, while help maintain the ionic and chemical environment. a. Schwann cells; astrocytes b. oligodendroglia; astrocytes c. oligodendroglia; microglia d. Schwann cells; microglia Answer: b Textbook Reference: Cells of the Nervous System 20. The primary immune response in the CNS comes from the action of a. microglia. b. astrocytes. c. white blood cells. d. oligodendroglia.

Answer: a Textbook Reference: Cells of the Nervous System

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21. Neural transmission is generally within a single neuron and between neurons. a. chemical; electrical b. electrical; electrical c. electrical; chemical d. chemical; chemical Answer: c Textbook Reference: Electrical Transmission within a Neuron 22. The is best described as a result of the selective permeability of the neuronal membrane and the uneven distribution of ions inside and outside the cell. a. action potential b. threshold c. local potentials d. resting membrane potential Answer: d Textbook Reference: Electrical Transmission within a Neuron 23. The Na+/K + pump helps to maintain the by moving three Na+ ions in and + two K ions out of the cell. a. action potential b. resting membrane potential c. threshold d. local potential Answer: b Textbook Reference: Electrical Transmission within a Neuron 24. The term ―hyperpolarization‖ refers to a. an excitatory postsynaptic potential. b. the opening of sodium channels. c. movement of the resting membrane potential closer to threshold. d. movement of the resting membrane potential farther from threshold.

Answer: d Textbook Reference: Electrical Transmission within a Neuron 25. Postsynaptic potentials are a type of potential. a. action b. local c. resting d. equilibrium Answer: b Textbook Reference: Electrical Transmission within a Neuron 26. At the equilibrium potential, the two forces acting on ions are in balance. These forces are the and the . + + a. Na /K pump; threshold

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b. Na+/K+ pump; electrostatic gradient c. concentration gradient; action potential d. concentration gradient; electrostatic gradient Answer: d Textbook Reference: Electrical Transmission within a Neuron 27. Excitatory postsynaptic potentials are generally caused by while inhibitory postsynaptic potentials may be caused by a. Na+; Cl– b. K+; Cl– c. Ca2+; K + d. Cl– ; K+ Answer: a Textbook Reference: Electrical Transmission within a Neuron

channels opening, channels opening.

28. Which statement about local potentials is false? a. They are generated on the dendrites and cell body. b. They occur only if threshold is reached. c. They move passively along the membrane. d. They are integrated at the axon hillock.

Answer: b Textbook Reference: Electrical Transmission within a Neuron 29. Summation of local potentials can lead to a(n) at the axon hillock if the is reached. a. equilibrium potential; threshold b. local potential; equilibrium potential c. action potential; equilibrium potential d. action potential; threshold Answer: d Textbook Reference: Electrical Transmission within a Neuron 30. Action potentials are first generated at the axon hillock because this is where are located. a. non-gated K + channels b. voltage-gated Na+ channels c. transporters d. Na+/K+ pumps Answer: b Textbook Reference: Electrical Transmission within a Neuron 31. During the a. absolute refractory b. conduction c. integration d. relative refractory

period, no additional action potentials can be created.

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Answer: a Textbook Reference: Electrical Transmission within a Neuron 32. The absolute refractory period occurs because channels cannot be opened, and the relative refractory period occurs because . a. voltage-gated Na+; voltage-gated K+ channels cannot be opened b. voltage-gated K+; voltage-gated Na+ channels remain open c. voltage-gated Na+; voltage-gated K+ channels remain open d. voltage-gated Na+; Na+/K+ pumps are activated Answer: c Textbook Reference: Electrical Transmission within a Neuron 33. Which statement about action potentials is false? a. They are considered all-or-none. b. Extreme excitation will result in a very large action potential. c. They can move via saltatory conduction in myelinated axons. d. They are generated at the axon hillock.

Answer: b Textbook Reference: Electrical Transmission within a Neuron 34. Local anesthetics, such as lidocaine, have their effects by a. blocking the Na+/K+ pump. b. preventing the generation of EPSPs and IPSPs. c. blocking voltage-gated Ca2+ channels. d. blocking voltage-gated Na+ channels.

Answer: d Textbook Reference: Electrical Transmission within a Neuron 35. The and nervous system are components of the peripheral nervous system and relay information about the internal and external environment, respectively. a. cranial nerves; somatic b. autonomic nervous system; sympathetic c. sympathetic nervous system; parasympathetic d. autonomic nervous system; somatic Answer: d Textbook Reference: Organization of the Nervous System 36. Which of the following is not part of the peripheral nervous system? a. Sympathetic nervous system b. Parasympathetic nervous system c. Spinal cord d. Cranial nerves Answer: c Textbook Reference: Organization of the Nervous System 37. A

section of the brain is cut parallel to the face.

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a. sagittal b. coronal c. horizontal d. caudal Answer: b Textbook Reference: Organization of the Nervous System 38. What kind of information is carried by the ventral roots of the spinal cord? a. Sensory information from muscles and skin b. Proprioceptive information from joints and muscles c. Motor information to muscles d. Motor and sensory information Answer: c Textbook Reference: Organization of the Nervous System 39. The sympathetic nervous system is responsible for as its neurotransmitter(s). a. energy conservation; acetylcholine b. energy conservation; acetylcholine and norepinephrine c. fight-or-flight; acetylcholine d. fight-or-flight; acetylcholine and norepinephrine Answer: d Textbook Reference: Organization of the Nervous System

functions and uses

40. Clusters of cell bodies in the CNS are called _ , and their associated bundles of axons are called . a. nuclei; tracts b. ganglia; tracts c. nuclei; nerves d. ganglia; nerves Answer: a Textbook Reference: Organization of the Nervous System

Matching 41. Match each numbered description with a lettered term below.

1. Releases acetylcholine at ganglia and target 2. Fluid-filled cavities in the brain 3. Brain structure that regulates respiration and heart rate 4. Part of diencephalon involved in regulating homeostasis 5. Neural network that regulates motivation and emotion 6. Brain structure that connects right and left hemispheres 7. Originates in thoracic and lumbar spinal cord 8. Part of brain that process and relays sensory information to cortex

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a. Limbic system b. Corpus callosum c. Hypothalamus d. Parasympathetic division e. Thalamus f. Sympathetic division g. Cerebral ventricles h. Medulla Answer: 1. d; 2. g; 3. h; 4. c; 5. a; 6. b; 7. f; 8. e Textbook Reference: Organization of the Nervous System

Short Answer/Essay 42. Write a coherent and informative paragraph using the following terms: transcription factor, promoter region, transcription, translation.

Answer: Changes in synaptic activity increase or decrease the production of particular proteins by activating transcription factors in the nucleus. Transcription factors are nuclear proteins that direct protein production. Transcription factors such as CREB bind to the promoter region of the gene adjacent to the coding region, modifying its rate of transcription. Transcription occurs in the nucleus, where messenger RNA (mRNA) makes a complementary copy of the active gene. After moving from the nucleus to the cytoplasm, mRNA attaches to organelles called ribosomes, which decode the ―recipe‖ and link the appropriate amino acids together to form the protein. This process is called translation.

Textbook Reference: Cells of the Nervous System 43. Briefly describe the role of chromatin remodeling in the epigenetic modification of gene expression.

Answer: Chromatin is a complex of DNA, histone proteins, and nonhistone proteins.

When histone tails are acetylated, charges open up the chromatin, creating an active state that allows transcription factors to bind to the promoter region of a gene to enhance transcription. The inactive state of chromatin is caused by methylation of histone tails, which pulls the chromatin tighter and prevents the binding of transcription factors, reducing transcription of the gene.

Textbook Reference: Cells of the Nervous System 44. Name four types of glial cells and give at least one function of each type.

Answer: Schwann cells and oligodendroglia produce myelin sheath on peripheral and central nervous system neurons, respectively. Astrocytes regulate the extracellular environment of the neurons, regulate CNS blood flow, and provide physical support and nutritional assistance. Microglia act as phagocytes to remove cellular debris and provide immune function.

Textbook Reference: Cells of the Nervous System 45. How are local potentials and action potentials similar, and how are they different?

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Answer: Similarities: Both involve Na+ and K+ channels. Differences: Local potentials are graded, decremental, produced by opening of ligand -gated ion channels, involve depolarization or hyperpolarization, and spatial and temporal summation. Action potentials are ―all-or-none,‖ nondecremental, produced by opening of voltage-gated channels, involve depolarization only, and the intensity of stimulus is coded by rate of firing.

Textbook Reference: Electrical Transmission within a Neuron 46. Give a detailed, step-by-step description of the stages of an action potential, including a description of and explanation for the refractory periods.

Answer: The summation of all EPSPs and IPSPs occurring at any single moment in time occurs at the axon hillock. If the threshold is reached (usually approximately a change from –70 mV to –50 mV), voltage-gated Na+ channels open, allowing large amounts of Na+ to enter the axon to produce the massive depolarization known as the action potential. At the peak of the action potential (+40 mV), voltage-gated Na+ channels close and cannot be opened until they reset at the resting potential, so no action potential can occur during this time (this is called the absolute refractory period). As the cell becomes more positive inside, voltage-gated K + channels open and K + exits from the cell, bringing the membrane potential back toward resting levels. The overshoot by K + causes the cell to be more polarized than normal, so it is more difficult (although still possible) to reach the threshold to generate another action potential relative refractory period). The action potential moves down the length of the axon by sequential opening of voltage-gated Na+ channels.

Textbook Reference: Electrical Transmission within a Neuron 47. Compare and contrast the sympathetic and parasympathetic divisions of the autonomic nervous system.

Answer: The sympathetic nervous system predominates when energy expenditure is necessary, such as during times of stress, excitement, and exertion. This system increases heart rate and blood pressure, stimulates secretion of adrenaline, and increases blood flow to skeletal muscles, among other effects. The parasympathetic division predominates at times when energy reserves can be conserved and stored for later use; this system increases salivation, digestion, and storage of glucose and other nutrients and also slows heart rate and decreases respiration.

Textbook Reference: Organization of the Nervous System 48. Discuss the anatomical differences between the sympathetic and parasympathetic divisions of the autonomic nervous system, including their points of origin in the central nervous system.

Answer: The cell bodies of sympathetic neurons are in the ventral horn at the thoracic and lumbar regions. Their axons project for a relatively short distance before they synapse with a cluster of cell bodies called sympathetic ganglia. The preganglionic fibers release acetylcholine onto cell bodies in the ganglia. The postganglionic cells project their axons for a relatively long distance to the target tissues and release norepinephrine. The cell bodies of the parasympathetic neurons are located either in the brain (cranial nerves) or in the ventral horn of the spinal cord at the sacral region. Preganglionic neurons travel long

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distances to synapse on cells in the parasympathetic ganglia are close to target organs and both preganglionic and postganglionic fibers release acetylcholine.

Textbook Reference: Organization of the Nervous System 49. Describe the HPA axis and the neuroendocrine stress response, including the idea of negative feedback.

Answer: Stress causes the secretion of corticotropin-releasing factor (CRF) by the paraventricular nucleus of the hypothalamus into the blood vessels ending in the anterior pituitary. The binding of CRF in that gland causes the release of adrenocorticotropic hormone (ACTH) into the general blood circulation. ACTH subsequently binds to the adrenal cortex to increase the secretion of cortisol and other glucocorticoids, all of which contribute to the mobilization of energy to cope with stress or exertion. Cortisol feeds back to the hypothalamus (and hippocampus) to shut down HPA activation and return cortisol levels to normal.

Textbook Reference: Organization of the Nervous System 50. Name and briefly describe the functions of the four lobes of the cerebral cortex.

Answer: The frontal lobe is responsible for movement and executive function. The other three lobes are sensory in function: parietal (somatosensory—touch, temperature, pain); occipital (vision); and temporal (audition).

Textbook Reference: Organization of the Nervous System

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Test Bank to accompany

Psychopharmacology, Third Edition Meyer • Quenzer

Chapter 3: Chemical Signaling by Neurotransmitters and Hormones Multiple Choice 1. Otto Loewi’s experiment with frog hearts was important because it demonstrated that a. the idea of chemical neurotransmission is correct. b. electrical impulses are responsible for neural transmission. c. the frog heart can be kept alive when removed from the frog. d. the neuron doctrine is correct.

Answer: a Textbook Reference: Introduction 2. The most common type of synapse in the brain is the a. axoaxonic b. axodendritic c. axosomatic d. presynaptic inhibition Answer: b Textbook Reference: Chemical Signaling between Nerve Cells

synapse.

3. Though he could not see it, Sir Charles Sherrington correctly surmised that neurons do not actually touch one another. This idea has been verified with the use of a. the electron microscope. b. the light microscope. c. frog heart experiments first done by Loewi. d. electrophysiological recordings.

Answer: a Textbook Reference: Chemical Signaling between Nerve Cells 4. The sac-like structures in the presynaptic terminal are called with . a. mitochondria; neurotransmitter molecules b. synaptic vesicles; mitochondria c. synaptic vesicles; neurotransmitter molecules d. mitochondria; ATP Answer: c Textbook Reference: Chemical Signaling between Nerve Cells

and are filled

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5. Which of the following is not one of the criteria a substance must meet to be considered a neurotransmitter? a. A synthetic mechanism is present in the presynaptic cell. b. Vesicles containing the substance move down the axon with the action potentials when the neuron is stimulated. c. Receptors for the proposed substance are present on the postsynaptic cell. d. There is a means for inactivating the substance.

Answer: b Textbook Reference: Neurotransmitter Synthesis, Release, and Inactivation 6. If a substance is a neurotransmitter, stimulation of the presynaptic cell should have the same effect as a. direct application of the proposed substance to the postsynaptic cell. b. stimulation of the postsynaptic cell. c. blocking receptors on the postsynaptic cell. d. inactivating the substance.

Answer: a Textbook Reference: Neurotransmitter Synthesis, Release, and Inactivation 7. Activity at an axoaxonic synapse can directly increase the amount of neurotransmitter released from the postsynaptic cell. This is known as a. presynaptic inhibition. b. neuromodulation. c. axosomatic activation. d. presynaptic facilitation.

Answer: d Textbook Reference: Neurotransmitter Synthesis, Release, and Inactivation 8. The classical neurotransmitters do not include a. acetylcholine. b. amino acids. c. neuropeptides. d. monoamines.

Answer: c Textbook Reference: Neurotransmitter Synthesis, Release, and Inactivation 9. If one neuron contains both a neuropeptide and a classical neurotransmitter, a. all vesicles in the neuron will contain both substances. b. stimulation of the neuron will result in release of only one of these. c. some vesicles will contain only the neuropeptide and other vesicles will contain both substances. d. some vesicles will contain only the classical neurotransmitter and other vesicles will contain both substances.

Answer: d Textbook Reference: Neurotransmitter Synthesis, Release, and Inactivation

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10. Which statement about neuropeptides is false? a. Neuropeptide replenishment after neural activity occurs more slowly than replenishment of classical neurotransmitters. b. Neuropeptides must be synthesized in the cell body. c. Necessary enzymes are packed into the vesicle with the protein precursor. d. Transport of the vesicles down the axon depends on action potential propagation.

Answer: d Textbook Reference: Neurotransmitter Synthesis, Release, and Inactivation 11. The direct effect of depolarization of the presynaptic nerve terminal by the action potential is the a. docking of vesicles at the active zones. b. opening of voltage-gated Ca2+ channels. c. packaging of neurotransmitter into vesicles. d. activation of autoreceptors.

Answer: b Textbook Reference: Neurotransmitter Synthesis, Release, and Inactivation 12. The process of releasing neurotransmitter molecules from the vesicles is known as and occurs as a result of an influx of . a. exocytosis; Ca2+ b. endocytosis; Ca2+ c. exocytosis; Na+ d. docking; K+ Answer: a Textbook Reference: Neurotransmitter Synthesis, Release, and Inactivation 13. Prior to neurotransmitter release, vesicles are transported to specialized regions of the presynaptic terminal called zones, where they bind to the terminal in a process known as . a. priming; docking b. active; docking c. active; endocytosis d. priming; exocytosis Answer: b Textbook Reference: Neurotransmitter Synthesis, Release, and Inactivation 14. Which statement about vesicular recycling is false? a. It occurs through a process known as endocytosis. b. Without it, the neuron would grow progressively larger as vesicular membrane is added to the terminal. c. New vesicles for classical neurotransmitters and neuropeptides are re-formed and filled in the terminal. d. The processes of endocytosis and exocytosis constitute vesicle recycling.

Answer: d Textbook Reference: Neurotransmitter Synthesis, Release, and Inactivation

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15. When activated, somatodendritic autoreceptors a. increase neurotransmitter release. b. increase the rate of cell firing. c. reduce the rate of cell firing. d. reduce neurotransmitter release.

Answer: c Textbook Reference: Neurotransmitter Synthesis, Release, and Inactivation 16. Selective blockade of terminal autoreceptors for DA would lead to a(n) a. increase in neurotransmitter release. b. decrease in neurotransmitter release. c. decrease in cell firing. d. increase in cell firing.

Answer: a Textbook Reference: Neurotransmitter Synthesis, Release, and Inactivation 17. Inactivation of neurotransmitters cannot be accomplished by a. enzymatic breakdown in the synaptic cleft. b. transport back into the presynaptic cell. c. transport into the postsynaptic cell. d. transport into nearby glial cells.

Answer: c Textbook Reference: Neurotransmitter Synthesis, Release, and Inactivation 18. Cocaine increases the amount of DA, 5-HT, and NE in the synaptic cleft by a. preventing metabolism. b. blocking transporters. c. blocking autoreceptors. d. increasing synthesis.

Answer: b Textbook Reference: Neurotransmitter Synthesis, Release, and Inactivation 19. The specific effect of a particular neurotransmitter at a particular synapse is largely determined by a. the receptor subtype(s) present on the postsynaptic cell. b. the rate of firing of the presynaptic cell. c. reuptake and metabolism of the neurotransmitter. d. the presence of antagonists at the synapse.

Answer: a Textbook Reference: Neurotransmitter Receptors and Second-Messenger Systems 20. Which statement about ionotropic receptors is true? a. They rapidly cause intracellular effects. b. G proteins are activated upon binding of neurotransmitter. c. They are composed of only one subunit.

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d. Binding of an agonist induces long-lasting responses in the cell.

Answer: a Textbook Reference: Neurotransmitter Receptors and Second-Messenger Systems 21. Ionotropic receptors may let in , which can then act as a(n) . a. Na+; second messenger b. Ca2+; kinase c. Ca2+; second messenger d. Cl– ; effector enzyme Answer: c Textbook Reference: Neurotransmitter Receptors and Second-Messenger Systems 22. Ligand-gated ion channels are ; G protein–coupled receptors are a. slow/ionotropic; fast/metabotropic b. fast/ionotropic; slow/metabotropic c. slow/metabotropic; fast/ionotropic d. fast/metabotropic; slow/ionotropic Answer: b Textbook Reference: Neurotransmitter Receptors and Second-Messenger Systems

.

23. Which statement regarding metabotropic receptors is false? a. The receptor itself is an ion channel that opens upon ligand binding. b. The receptor has one subunit with seven transmembrane domains. c. They are coupled to intracellular G proteins. d. When activated they can stimulate effector enzymes.

Answer: a Textbook Reference: Neurotransmitter Receptors and Second-Messenger Systems 24. Synaptic inhibition may be produced by ACh acting through metabotropic receptors.

This inhibition results from the activation of channels by the G protein. + a. Na b. Cl– c. K+ d. Ca2+ Answer: c Textbook Reference: Neurotransmitter Receptors and Second-Messenger Systems 25. Activating a metabotropic receptor cannot result in a. opening of a G protein–gated ion channel. b. changes in the levels of a second messenger. c. opening of an ion channel within the receptor. d. changes in gene expression.

Answer: c Textbook Reference: Neurotransmitter Receptors and Second-Messenger Systems

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26. Which of the following best describes the sequence of steps following the activation of a metabotropic receptor? a. Activation of G protein → change in activity of effector enzyme → activation of protein kinase → change in second messenger levels b. Activation of G protein → change in second messenger levels → change in activity of effector enzyme → activation of protein kinase c. Change in second messenger levels → change in activity of effector enzyme → activation of protein kinase → activation of G protein d. Activation of G protein → change in activity of effector enzyme → change in second messenger levels → activation of protein kinase Answer: d Textbook Reference: Neurotransmitter Receptors and Second-Messenger Systems 27. receptors mediate the effects of neurotrophic factors. a. Calcium/calmodulin kinase b. Tyrosine kinase c. Protein kinase A d. Protein kinase C Answer: b Textbook Reference: Neurotransmitter Receptors and Second-Messenger Systems 28. In contrast to the classical neurotransmitters and the neuropeptides, nitric oxide does not ―behave‖ like a typical neurotransmitter. Which statement regarding nitric oxide signaling is false? a. It may be released from the postsynaptic cell. b. It is not released from synaptic vesicles via exocytosis. c. It remains in the synaptic cleft until it is inactivated. d. It may travel some distance before it reaches target cells.

Answer: d Textbook Reference: Neurotransmitter Receptors and Second-Messenger Systems 29. The relaxing effects of on smooth muscle and the resulting dilation of the arteries are due to an increase in the second messenger . a. protein kinase G; cGMP b. protein kinase A; cAMP c. nitric oxide; cGMP d. nitric oxide; calcium Answer: c Textbook Reference: Neurotransmitter Receptors and Second-Messenger Systems 30. Neurotrophic factors are generally involved in regulating a. long term changes, such as gene expression. b. the rate of cell firing. c. rapid synaptic events. d. opening of ion channels.

Answer: a

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Textbook Reference: Neurotransmitter Receptors and Second-Messenger Systems 31. Binding of neurotrophic factors to their respective trk receptors results in the a. activation of G proteins. b. reciprocal phosphorylation of the two receptor molecules. c. opening of ion channels. d. activation of second messenger systems.

Answer: b Textbook Reference: Neurotransmitter Receptors and Second-Messenger Systems 32. The primary treatment for Parkinson’s disease is the administration of L-DOPA because this drug a. stimulates the release of dopamine. b. inhibits the synthesis of dopamine. c. directly stimulates postsynaptic dopamine receptors. d. is the synthetic precursor to dopamine.

Answer: d Textbook Reference: Pharmacology of Synaptic Transmission 33. Environmental stimuli, sensory stimuli, and psychoactive drugs can trigger longlasting changes in neuronal connectivity. Collectively, these changes are termed a. synaptic plasticity. b. dendritic spine plasticity. c. synaptic density. d. sensitization.

Answer: a Textbook Reference: Synaptic Plasticity 34. Neurotransmitters are released into the the . a. synaptic cleft; brain b. bloodstream; synaptic cleft c. synaptic cleft; bloodstream d. vesicles; bloodstream Answer: c Textbook Reference: The Endocrine System

, whereas hormones are released into

35. is an example of a substance that can act as both a neurotransmitter and a hormone. a. Acetylcholine b. Norepinephrine c. Nitric oxide d. Cortisol Answer: b Textbook Reference: The Endocrine System

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36. In response to stressors, the adrenal cortex secretes secretes . a. epinephrine; norepinephrine b. epinephrine; glucocorticoids c. glucocorticoids; chromaffin cells d. glucocorticoids; epinephrine Answer: d Textbook Reference: The Endocrine System

and the adrenal medulla

37. Secretory neurons from the hypothalamus release bloodstream from the pituitary. a. prolactin; vasopressin; anterior b. vasopressin; oxytocin; posterior c. oxytocin; prolactin; posterior d. releasing hormones; tropic; anterior Answer: b Textbook Reference: The Endocrine System

and

_ into the

38. Releasing hormones from the enter the bloodstream in the median eminence and act on the , causing the release of various hormones. a. anterior pituitary; thyroid b. posterior pituitary; hypothalamus c. hypothalamus; anterior pituitary d. hypothalamus; posterior pituitary Answer: c Textbook Reference: The Endocrine System 39. Which statement regarding hormones and neuropharmacology is false? a. Hormones can alter behavioral responses to drugs. b. Hormone secretion can be altered by psychoactive drugs. c. Some hormones have psychoactive effects on their own. d. The effects of hormones on the brain are simple and easy to measure.

Answer: d Textbook Reference: The Endocrine System 40. Steroid hormones bind to receptors, which act as and regulate gene expression. a. metabotropic; G proteins b. intracellular; transcription factors c. tyrosine kinase; transcription factors d. membrane-bound; G proteins Answer: b Textbook Reference: The Endocrine System

when activated,

Matching

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41. Match each numbered description with a lettered term below.

1. May occur at axoaxonic synapses 2. Provide(s) feedback to decrease neurotransmitter release 3. Release(s) norepinephrine and epinephrine 4. Amplifies chemical signal with second messengers 5. Move(s) neurotransmitter into terminal 6. The ―master gland‖ 7. Associated with cyclic AMP a. Metabotropic receptors b. Protein kinase A c. Pituitary d. Presynaptic inhibition e. Autoreceptors f. Transporters g. Chromaffin cells Answer: 1. d; 2. e; 3. g; 4. a; 5. f; 6. c; 7. b Textbook Reference: Neurotransmitter Synthesis, Release, and Inactivation

Short Answer/Essay 42. Describe three factors that regulate neurotransmitter release.

Answer: Any three of the following: (Answers may vary.)

• The rate of cell firing—the more rapid the firing, the greater the NT release.

• The probability of neurotransmitter release—synapses in different parts of the brain vary in the probability that even a single vesicle will undergo exocytosis in response to an action potential.

• The presence of autoreceptors on axon terminals or cell bodies and dendrites— terminal autoreceptors, located on axon terminals, typically inhibit further transmitter release; somatodendritic autoreceptors, on the cell body or dendrites, slow the rate of cell firing, resulting in less neurotransmitter release because fewer action potentials reach the axon terminal to stimulate NT release.

• Agonist or antagonist drugs—stimulate or block autoreceptors.

• Heteroreceptors—respond to transmitters other than the main NT for that synapse and may enhance or reduce the amount of transmitter released from axon terminal.

Textbook Reference: Neurotransmitter Synthesis, Release, and Inactivation 43. List the criteria for classifying a substance as a neurotransmitter.

Answer: Any or all of the following: (Answers may vary.)

• The presynaptic cell should contain the proposed substance along with a mechanism for manufacturing it.

• A mechanism for inactivating the substance should also be present.

• The substance should be released from the axon terminal upon stimulation of the neuron.

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• •

Receptors for the proposed substance should be present on the postsynaptic cell.

Direct application of the proposed substance or of an agonist drug that acts on its receptors should have the same effect on the postsynaptic cell as stimulating the presynaptic neuron does.

• Applying an antagonist drug that blocks the receptors should inhibit both the action of the applied substance and the effect of stimulating the presynaptic neuron.

Textbook Reference: Neurotransmitter Synthesis, Release, and Inactivation 44. Describe three types of symptoms typically associated with narcolepsy.

Answer: Cataplexy—sudden loss of muscle tone; hypnagogic hallucinations—vivid dream like sensations; sleep paralysis—loss of muscle tone leading to a sense of paralysis.

Textbook Reference: Neurotransmitter Synthesis, Release, and Inactivation 45. What role might orexin play in narcolepsy? Briefly explain evidence that supports this role.

Answer: Orexin may play a role in arousal and maintaining wakeful behavior.

Wakefulness can be stimulated in mice by activating orexin neurons. Dogs with narcolepsy have a mutation in a particular orexin gene, causing production of an abnormal OX2R protein and loss of normal postsynaptic responsiveness to orexin. In humans that have narcolepsy there appears to be a complete loss of orexin neurons throughout the hypothalamic area, suggesting that there is little to no orexin input to their sleep–waking circuits.

Textbook Reference: Neurotransmitter Synthesis, Release, and Inactivation 46. Compare and contrast metabotropic and ionotropic receptors.

Answer: Ionotropic receptors have 4–5 subunits that are assembled and then inserted into the cell membrane, whereas metabotropic receptors have just one subunit. Ionotropic receptors contain an intrinsic ion channel that opens in response to neurotransmitter or drug binding, whereas metabotropic receptors activate G proteins in response to neurotransmitter or drug binding. Ionotropic receptors are not coupled to second messengers but metabotropic receptors are. Ionotropic receptors are fast but metabotropic receptors are slower.

Textbook Reference: Neurotransmitter Receptors and Second-Messenger Systems 47. Briefly summarize five mechanisms by which drugs can alter synaptic transmission, and provide an example of a drug that acts in each manner.

Answer: Any five of the following: (Answers may vary.)

• Increase the rate of NT synthesis. Example: L-DOPA is the precursor to dopamine—increases synthesis of dopamine; used to treat Parkinson’s disease.

• Decrease the levels of neurotransmitter synthesized, such as by inhibiting enzymes needed for NT synthesis. Example: AMPT (alpha-methyl-para-tyrosine) inhibits the enzyme tyrosine hydroxylase, so synthesis of DA and NE is reduced.

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•

Enhance the activity of a neurotransmitter by blocking the enzyme that breaks the NT down. Example: Physostigmine blocks the enzyme acetylcholinesterase, which breaks down ACh, so more ACh remains in the synapse.

• Enhance the activity of a neurotransmitter (if it uses transporters for reuptake) by blocking the transporter that moves NT from the synapse back into the presynaptic terminal, thus increasing action in the synapse. Example: Cocaine blocks the transporter for DA, NE, and 5-HT. • Increase release of certain neurotransmitters from cytoplasm in axon terminal.

Example: Amphetamine stimulates the release of DA and NE. • Drugs that act on postsynaptic receptors for a specific neurotransmitter. Agonists mimic the neurotransmitter. Example: Opiates like heroin bind to opiate receptors and act like endogenous opiates. Antagonists block the neurotransmitter action in some way. Example: Caffeine blocks the action of adenosine at its receptors (without stimulating them).

Textbook Reference: Pharmacology of Synaptic Transmission 48. Write a coherent and informative paragraph using the following terms: hypothalamus; posterior pituitary; median eminence; releasing hormones.

Answer: The pituitary stalk, connecting the hypothalamus with the pituitary gland, contains blood vessels that carry special hypothalamic releasing hormones. These hormones are mainly neuropeptides manufactured by various groups of neurons in the hypothalamus. Instead of forming normal synapses, these neurons release peptides into blood capillaries in a region called the median eminence. These blood vessels carry the hormones to the hormone secreting regions of the anterior pituitary gland. The pituitary stalk also contains the axons of secretory neurons of the hypothalamus that synthesize the peptide hormones vasopressin and oxytocin. When these axons reach the posterior pituitary, they release these hormones into the bloodstream.

Textbook Reference: The Endocrine System 49. Describe how drugs that block the D2 dopamine receptor alter prolactin levels and release.

Answer: Release of the hormone prolactin is inhibited by the neurotransmitter DA (via its action on D 2 receptors in the pituitary gland). Several drugs that are used to treat psychiatric disorders, particularly schizophrenia, are D 2 receptor antagonists. One consequence of these drugs, therefore, is that the inhibitory effect of DA is removed, which results in a rise in blood prolactin levels.

Textbook Reference: The Endocrine System 50. Describe the evidence supporting the role of sex hormones in sensitivity to cocaine.

Answer: There is some evidence that sex hormone levels affect the intensity or subjective response to cocaine in women. Women who were tested during the midfollicular phase (6–10 days after the beginning of menstruation) and the midluteal phase (7–12 days following the LH surge) of their cycle reported lower intensity responses during their luteal phase than during their follicular phase. Men tested under the same conditions showed a response similar to that of women in their follicular phase.

Textbook Reference: The Endocrine System

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Test Bank to accompany

Psychopharmacology, Third Edition Meyer • Quenzer

Chapter 4: Methods of Research in Psychopharmacology Multiple Choice 1. Which statement about methods of research in neurobehavioral pharmacology is false? a. Use of scientific method and critical reading of literature are necessary skills. b. Methods focus only on the molecular level, not the whole organism. c. Researchers must be able to quantify changes in behavior, mood, and thinking. d. Many studies require images of neurotransmitters and receptors in the living brain.

Answer: b Textbook Reference: Research Methods for Evaluating the Brain and Behavior 2. Which statement about the importance of behavioral measures in psychopharmacology is false? a. Behavioral measures use observational measures, which are the most reliable and valid approaches. b. Behavioral measures are used for developing animal models of psychiatric disorders. c. Behavioral measures are used for screening newly-developed drug molecules in preclinical trials. d. Behavioral measures aid in understanding the neurochemical basis of behavior.

Answer: a Textbook Reference: Evaluating Animal Behavior 3. Which of the following is not an advantage of animal studies in psychopharmacology? a. They allow for precise control of living conditions not possible with humans. b. Assessing emotional and psychological changes in response to experimental manipulations is relatively straightforward in nonhuman subjects. c. The past histories of animal subjects are known to the investigator. d. Invasive procedures that would be unethical on humans can be used.

Answer: b Textbook Reference: Evaluating Animal Behavior 4. What are the limitations to studying fetal alcohol syndrome (FAS) in human subjects? a. There are not enough cases to study. b. The studies are correlational only; one cannot assert that alcohol causes any particular effect. c. There is very little evidence for FAS in children born to women in the United States. d. It is impossible to obtain permission to conduct this type of research.

Answer: b Textbook Reference: Evaluating Animal Behavior

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5. Which of the following is not a guideline of the Health Extension Act of 1985? a. Researchers should be trained in basic veterinary care. b. Alternative methods, such as computer simulation, should be considered. c. Procedures must avoid or minimize distress or pain. d. Research must benefit society or advance knowledge.

Answer: a Textbook Reference: Evaluating Animal Behavior 6. Good behavioral tests for drug effects should meet a variety of criteria. Which of the following is not one of these criteria? a. They should be specific for the drug class being screened. b. They should have face validity. c. They should be reliable. d. They should be sensitive, and show the same rank order of potency as seen in therapeutic action.

Answer: b Textbook Reference: Evaluating Animal Behavior 7. The is a test of analgesia. a. open field test b. catalepsy test c. tail-flick test d. multiple T-maze Answer: c Textbook Reference: Evaluating Animal Behavior 8. Which of the following is not a test for learning and memory? a. Morris water maze b. T-maze c. Light–dark crossing task d. Delayed-response test Answer: c Textbook Reference: Evaluating Animal Behavior 9. Which pair of behavioral test and what it is designed to measure is incorrectly matched? a. Delayed-response test: fear b. Conditioned place preference: reward c. Elevated plus-maze: anxiety d. Conditioned emotional response: fear Answer: a Textbook Reference: Evaluating Animal Behavior 10. Animals will not self-administer a. cocaine.

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b. nicotine. c. antidepressants. d. morphine.

Answer: c Textbook Reference: Evaluating Animal Behavior 11. Drug discrimination testing provides a way to observe a. how an organism experiences a drug. b. drug-induced euphoria. c. the motoric effects of a new therapeutic agent. d. the breaking point for a given drug.

Answer: a Textbook Reference: Evaluating Animal Behavior 12. In drug discrimination studies, which agent will produce the same lever-press response as that produced by training with morphine? a. Amphetamine b. Saline c. Methadone d. Marijuana Answer: c Textbook Reference: Evaluating Animal Behavior 13. In drug development and testing, a. animal testing occurs in phase I. b. the FDA reviews a new drug application after phase III clinical trials are complete. c. about 80% of drugs make it through to final approval. d. generic versions of a drug can be made 10 years after a drug is patented.

Answer: b Textbook Reference: Evaluating Animal Behavior 14. Which statement about translational research is false? a. It involves the transfer of discoveries from basic science research into clinical applications. b. One of its goals is to develop therapeutic drugs more quickly and inexpensively. c. It is facilitated by the development of parallel tasks and methods for animals and humans. d. It was developed recently—in the last decade.

Answer:d Textbook Reference: Evaluating Animal Behavior 15. Surgery using the stereotaxic apparatus a. is an in vitro procedure. b. can be used for the purpose of lesioning, microinjection, or recording. c. is 100% reliable in placing the electrode at the target site.

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d. is no longer performed on small animals; it has been replaced by use of the halo bracket device.

Answer: b Textbook Reference: Multiple Neurobiological Techniques for Assessing the CNS 16. How do researchers know the proper location to place electrodes or cannulae in the brains of animals? a. They use an atlas and landmarks on the animal’s skull. b. They use a trial and error process based on their own prior studies. c. They guide the electrode with MRI or CT scans. d. The electrode is stimulated as it is moved until the expected response is found.

Answer: d Textbook Reference: Multiple Neurobiological Techniques for Assessing the CNS 17. Why is a neurotoxin lesion preferred over an electrolytic lesion? a. It is less painful to animals than the electrolytic lesion. b. It is easier to perform than the electrolytic lesion. c. It is more selective than the electrolytic lesion because it destroys cell bodies only. d. It has a stronger, more easily detected behavioral effect than the electrolytic lesion.

Answer: c Textbook Reference: Multiple Neurobiological Techniques for Assessing the CNS 18. coordinate(s) is/are needed with stereotaxic surgery to specify a particular brain area. a. One b. Two c. Three d. Four Answer: c Textbook Reference: Multiple Neurobiological Techniques for Assessing the CNS 19. The halo bracket is used for brain surgery on a. mice. b. humans. c. rats. d. cats.

Answer: b Textbook Reference: Multiple Neurobiological Techniques for Assessing the CNS 20. If a researcher wants to disrupt a specific dopamine pathway, which method would be most effective? a. Electrolytic lesion b. Kainic acid c. Ibotenic acid d. 6-hydroxydopamine Answer: d

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Textbook Reference: Multiple Neurobiological Techniques for Assessing the CNS 21. In microdialysis, a. an animal is placed in a stereotaxic apparatus while measurements are taken. b. large quantities of fluid must be collected for HPLC analysis. c. analysis of the contents of the extracellular fluid can be made. d. chromatography separates substances only by ionic charge, and not by size.

Answer: c Textbook Reference: Multiple Neurobiological Techniques for Assessing the CNS 22. Which method uses microelectrodes to record the activity of neurochemicals in the extracellular fluid of freely moving animals? a. Microdialysis b. In vivo voltammetry c. Stereotaxic surgery d. Patch clamp electrophysiology Answer: b Textbook Reference: Multiple Neurobiological Techniques for Assessing the CNS 23. Macroelectrodes are used for all of the following except a. activating cells and generating action potentials. b. recording activity from thousands of neurons. c. controling tremors in Parkinson’s disease. d. quantifying receptor number and activation.

Answer: d Textbook Reference: Multiple Neurobiological Techniques for Assessing the CNS 24. Which statement about single-unit recording is false? a. It uses microelectrodes. b. It can involve intracellular recording. c. The animal must be anesthetized in all cases. d. The electrode is sometimes placed in the extracellular fluid.

Answer: c Textbook Reference: Multiple Neurobiological Techniques for Assessing the CNS 25. A technique that permits researchers to study the function of individual ion channels that are responsible for the action potential is a. in vivo voltammetry. b. patch clamp electrophysiology. c. intracellular recording. d. extracellular recording.

Answer: b Textbook Reference: Multiple Neurobiological Techniques for Assessing the CNS 26. With respect to identification of the location and quantity of neurochemicals in the brain,

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a. if location is the primary goal, then the brain slice method is preferred. b. if quantification is the main concern, researchers are most likely to preserve the intact tissue and prepare it with autoradiography. c. the ―soup‖ approach is most often used for localization of receptors. d. radioligand binding works better for the ―slice‖ method than the ―soup‖ method.

Answer: a Textbook Reference: Multiple Neurobiological Techniques for Assessing the CNS 27. Which of the following is not part of the procedure and/or interpretation of radioligand binding? a. Tissue is incubated with radioligand. b. Specificity is measured by adding radioactive competing ligand. c. Saturability is measured by adding increasing amounts of ligand. d. Reversibility is measured by showing displacement of ligand by drug.

Answer: b Textbook Reference: Multiple Neurobiological Techniques for Assessing the CNS 28. In radioligand binding studies, represents the number of binding sites and is an indication of receptor affinity. a. Bmax ; k1 b. k–1 ; Kd c. k1 ; k–1 d. Bmax ; Kd Answer: d Textbook Reference: Multiple Neurobiological Techniques for Assessing the CNS 29. Which statement regarding receptor autoradiography is false? a. It provides information about receptor number and location. b. It tells the researcher about the affinity of receptors for a particular drug in a certain region of the brain. c. It is useful for studying the effects of brain lesions on receptor binding. d. It cannot be used when the receptor binding has occurred in vivo.

Answer: d Textbook Reference: Multiple Neurobiological Techniques for Assessing the CNS 30. Neuropharmacologists are interested in enzymes for a variety of reasons. Which of the following is not one of the reasons? a. Enzymes can be identified with techniques such as receptor autoradiography. b. Enzymes are used to synthesize and metabolize neurotransmitters. c. Enymes regulate the levels of second messengers, such as cyclic AMP. d. Enzymes play a role in complex events, such as drug tolerance.

Answer: a Textbook Reference: Multiple Neurobiological Techniques for Assessing the CNS 31. In immunocytochemistry, a. tissue slices are cut and incubated with antigen in solution.

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b. the antibody response is not very selective because it recognizes a class of similar proteins. c. antibodies must initially be tested by injecting them into host animals. d. cells making the neuropeptide hypocretin can be visualized via creating tagged antibodies to the neuropeptide.

Answer: d Textbook Reference: Multiple Neurobiological Techniques for Assessing the CNS 32. Which procedure would be used for quantifying molecules in various body fluids and tissue extracts from unknown samples? a. Immunocytochemistry b. In situ hybridization c. Radioimmunoassay d. Autoradiography Answer: c Textbook Reference: Multiple Neurobiological Techniques for Assessing the CNS 33. In situ hybridization (ISH) is used a. for antibody labeling of proteins. b. for detection of messenger RNA molecules. c. to determine location and quantification of receptors. d. to measure second-messenger activity.

Answer: b Textbook Reference: Multiple Neurobiological Techniques for Assessing the CNS 34. Which statement about in situ hybridization is false? a. It is a very sensitive procedure in terms of its ability to detect mRNA. b. Tissue homogenate, as in the Northern blot or dot blot methods, can be used. c. It is used for global, but not regional, changes in mRNA over time. d. A probe of complementary base-pair sequences to the mRNA of interest is used.

Answer: c Textbook Reference: Multiple Neurobiological Techniques for Assessing the CNS 35. DNA microarrays are not used to a. quantify neurochemicals in the brain. b. aid in identification of the genes that switch on and off together in response to drugs and diseases. c. help scientists understand the many presynaptic proteins that are underexpressed in schizophrenia. d. make it possible to screen the entire genome using just a few chips.

Answer: a Textbook Reference: Multiple Neurobiological Techniques for Assessing the CNS 36. Which technique does not permit visualization of the living human brain? a. Functional MRI b. In situ hybridization (ISH)

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c. Computerized tomography d. SPECT Answer: b Textbook Reference: Multiple Neurobiological Techniques for Assessing the CNS 37. Researchers use 2-DG autoradiography to a. identify regions of the brain with high metabolic activity. b. locate c-fos expression in the brain. c. identify the presence of objects of different densities in the brain, such as a tumor. d. provide three dimensional images of the brain.

Answer: a Textbook Reference: Multiple Neurobiological Techniques for Assessing the CNS 38. Researchers who want to stain for cells that are actively expressing proteins should use a. 2-DG autoradiography. b. in vivo voltammetry. c. c-fos identification with ICC. d. computerized tomography.

Answer: c Textbook Reference: Multiple Neurobiological Techniques for Assessing the CNS 39. The CT scan a. provides a dynamic picture of the human brain. b. has better resolution than the MRI scan. c. requires that subjects be injected with a radioactively labeled substance. d. is based on a series of reconstructed X rays of the brain.

Answer: d Textbook Reference: Multiple Neurobiological Techniques for Assessing the CNS 40. One major advantage of the MRI scan is that a. it provides all the information that is needed in one slice. b. the images it provides offer incredible detail of the brain. c. it can show changes in brain activity over time. d. it can be used in conjunction with cognitive and behavioral tasks.

Answer: b Textbook Reference: Multiple Neurobiological Techniques for Assessing the CNS 41. Which statement about PET scans is false? a. They use radioisotopes that decay rapidly, emitting positrons in the process. b. They are used to detect where labeled drugs and transmitters might bind. c. They provide detailed structural information if the proper reagents are used. d. They can be used to determine which brain areas are active during cognitive tasks.

Answer: c Textbook Reference: Multiple Neurobiological Techniques for Assessing the CNS

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42. Which of the following is not a reason that functional MRI is preferred over PET imaging? a. The detail is far superior in functional MRI. b. The fMRI procedure provides both anatomical and functional information. c. The individual does not need to be injected with a radioactive substance in functional MRI. d. Because fMRI is a newer procedure, it has replaced the need for other techniques like PET and EEG. Answer: d Textbook Reference: Multiple Neurobiological Techniques for Assessing the CNS 43. Electroencephalography a. is an invasive method for measuring brain activity. b. measures action potentials from neurons. c. is often used to record ERPs or event-related potentials. d. can identify whether specific cells are active in sleep or waking.

Answer: c Textbook Reference: Multiple Neurobiological Techniques for Assessing the CNS 44. Which of the following is not a reason that we should be cautious about interpreting the findings from studies using transgenic mice? a. Complex behaviors and disorders are not controlled by single genes. b. Manipulating genes in mice does not give us useful information about systems in humans. c. A change in only one gene, the targeted mutation, may be masked by other compensating systems. d. Gene changes occur in all tissues at all stages of development.

Answer: b Textbook Reference: Multiple Neurobiological Techniques for Assessing the CNS 45. In one study, mice that were genetically engineered to express R6/2 (the Huntington’s disease gene) exhibited motor disturbances that _ and these mice also showed . a. improved over time; enhanced cognitive function b. were present from birth onward; a tendency to develop diabetes c. worsened over time; a shortened life span d. disappeared with practice; spatial learning deficits Answer: c Textbook Reference: Multiple Neurobiological Techniques for Assessing the CNS 46. Which statement about knockout mice is false? a. They are also called transgenic mice. b. They are a product of genetic engineering. c. They are bred from animals whose DNA has been altered to reflect the particular mutation.

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d. The knockout gene is often a gene for a receptor or enzyme involved in neurotransmitter synthesis or metabolism.

Answer: a Textbook Reference: Multiple Neurobiological Techniques for Assessing the CNS 47. When optogenetics is used to insert channelrhodopsin (ChR2) in a neuron, activating this protein with light will produce an of ions. a. efflux; chloride b. influx; chloride c. efflux; sodium d. influx; sodium Answer: d Textbook Reference: Multiple Neurobiological Techniques for Assessing the CNS

Short Answer/Essay 48. List three advantages that animal studies have over human studies.

Answer: Controls can be used that have uniform living conditions; history and genetic composition is known; and more substantial invasive techniques can be used to study drug mechanisms of action.

Textbook Reference: Evaluating Animal Behavior 49. Identify the three aspects of the Health Extension Act that exist to provide some protections for animals in research.

Answer: The research must be relevant to the benefit of human society; alternative approaches, such as computer simulations, must be considered; and procedures must minimize pain and discomfort.

Textbook Reference: Evaluating Animal Behavior 50. Explain what is meant by face, predictive, and construct validity. Which is most important for the development of clinically useful medications?

Answer: For animal disorder models, face validity means the traits observed in the model resemble those seen in the disorder. Predictive validity means that treatments that relieve abnormal traits seen in the animal disorder model will also relieve these abnormal traits in the human disorder. Construct validity states that the etiology, or cause, of the abnormal traits in the animal model is the same as that for the human disorder (e.g., the same genetic mutation introduced into the animal as is seen in the human disorder).

Textbook Reference: Evaluating Animal Behavior 51. Identify several common behavioral measures of learning/memory and emotions.

Answer: For learning and memory: radial arm maze, Morris water maze, delayed response test. For emotions: light–dark crossing task, elevated plus-maze, fearpotentiated startle, learned helplessness.

Textbook Reference: Evaluating Animal Behavior

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52. Describe one of the operant conditioning paradigms that are often used to study the effects of drugs on the nervous system. What does the breaking point signify in selfadministration procedures?

Answer: One experiment involves a rat in a cage with two levers. One lever will deliver a saline solution when pressed, the other lever will deliver a drug such as cocaine. The rat learns the effects for both levers. The frequency with which the rat chooses the cocaine lever to self-administer the cocaine is recorded. The researcher can change how many lever presses are required to get an injection and record at what point the rat will stop pressing for the injection. That is called the breaking point. With cocaine, the breaking point would be very high (i.e., the rat will be willing to press the lever many times to get a cocaine injection). Drugs that have very high breaking points are often drugs that people will self-administer for recreational purposes, and may possess the ability to produce a drug addiction.

Textbook Reference: Evaluating Animal Behavior 53. Explain how drug discrimination training works and indicate why it is useful. Include specific examples in your answer.

Answer: Drug discrimination tests allow you to ―ask‖ a rat: does drug B feel like drug A? A researcher can train a rat to get a reward like food when, after an administration of amphetamine (drug A), for instance, it presses the right lever. On the other hand, the rat receives the food reward following saline administration when it presses the left lever.

This is repeated over several days. On the test day you administer drug B (for example, cocaine). If the rat presses the right lever, the one it associates with reward when getting amphetamine, this indicates that, to the rat, the cocaine feels like amphetamine. If drug B had been morphine, the rat would not press the right lever, since morphine would not feel like amphetamine. If the researcher started with morphine, she would find that on the test day, the rat would indicate that an injection of heroin feels like morphine.

Textbook Reference: Evaluating Animal Behavior 54. Explain how genetic manipulations, brain lesions, and parallel tasks are important for translational research. Make sure to explain what translational research is.

Answer: Translational research could be described as ―from bench to bedside.‖ It represents the goal of making use of basic science discoveries (at the bench) in order to provide new therapies for treating patients (at the bedside). With genetic manipulations, one can make animal models with genetic defects that match those seen in human genetic disorders. Brain lesions have been carried out in animals in an attempt to produce symptoms that are seen in human disorders. Treatments can then be tried in the animals to relieve these symptoms with the hope that successful treatment in the animals can lead to successful treatment in human patients. Parallel tasks refer to using the same methodologies in both animals and humans to try to increase the chance that a treatment that relieves symptoms in an animal disorder model will also work in humans. Example: using the stop-signal task in animals and humans as a measure of impulsivity, with the idea that treatments that reduce this trait in animals may also reduce impulsivity in humans with disorders such as attention deficit hyperactivity disorder (ADHD).

Textbook Reference: Evaluating Animal Behavior

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55. Describe how the procedure of stereotaxic surgery is used for the purpose of producing lesions. Compare the benefits and drawbacks of using electrolytic and neurotoxic lesions.

Answer: Using a stereotaxic apparatus, a researcher can locate any area in the brain using three coordinates describing the point in relation to a reference point by indicating how far from the reference point one needs to go with regard to lateral direction, rostral/caudal direction, and dorsal/ventral depth. He can then use an electrode to cause an electrolytic lesion in that area. One caveat: neurons in the area other than the target neurons may be dstroyed.

Textbook Reference: Multiple Neurobiological Techniques for Assessing the CNS 56. What type of activity is measured by macroelectrodes, microelectrodes, and patch clamp electrophysiology? Provide one clinical application and one research application of the use of macroelectrodes.

Answer: Macroelectrodes can be used to either measure activity in a brain area or to stimulate a particular brain area. One could, for instance, determine if stimulation in a specific brain area can cause analgesia. Clinically, implanted macroelectrodes have been used to reduce the symptoms of Parkinson’s disease. With microelectrodes, one can achieve single-cell recording, and with patch clamping one can examine individual ion channels.

Textbook Reference: Multiple Neurobiological Techniques for Assessing the CNS 57. Describe the procedure of microdialysis, list its advantages, and provide an example of how it might be used to study the nervous system.

Answer: Microdialysis measures transmitter release in the brain of an awake, behaving animal. Following stereotaxic surgery, a microdialysis probe can be inserted at a particular brain site. Fluid flows through the probe, and the probe contains dialysis tubing that will allow released transmitter to pass through and enter the fluid flow and be collected for measurement. This technique can be used to determine if amphetamine stimulates dopamine release in brain areas such as the nucleus accumbens or striatum.

Textbook Reference: Multiple Neurobiological Techniques for Assessing the CNS 58. Name and describe three methods that are used to visualize the quantity and location of receptors in the brain.

Answer: One methed uses radioactive ligand for the receptor and studies its binding in membrane preparations following tissue homogenization and differential centrifugation to isolate the membranes. Excess unlabeled ligand can be used to displace the saturable (specific) ligand binding to the receptor, and the residual binding (non-specific) would be subtracted from the binding in the absence of excess unlabeled ligand to determine the value for specific, saturable receptor binding. Autoradiography uses intact brain slices and carries out the procedure detailed above for membranes. Overlaying the tissue with photographic film allows the radioactive energy to develop the film where the radioactive ligand was bound, and this can gives a picture of where binding took place in the intact tissue. A thrid method involves injecting the radioactive ligand into the animal and then making slices of the brain to carry out the autoradiography procedure as described above.

This will show where the binding took place in vivo (in the live animal).

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Textbook Reference: Multiple Neurobiological Techniques for Assessing the CNS 59. Identify and describe the criteria that must be met if we are to assume that the radioligand is, in fact, binding to the target receptors.

Answer: Answers may vary.

• The binding should be to specific receptors. This can be shown by displacement of the radioactive ligand binding by unlabeled receptor ligands.

• The binding should be saturable. This can be shown by demonstrating that as the concentration of the ligand increases, the amount of binding levels off, at which point we would say that the binding has saturated.

• The binding should be reversible. Displacement by competing receptor ligands would show this.

• Biological relevance can be shown by determining if the affinity for binding of a series of ligands parallels their potency (sensitivity) in some biological test system in which they are active.

Textbook Reference: Multiple Neurobiological Techniques for Assessing the CNS 60. What does in situ hybridization (ISH) measure? Why would a researcher choose this method as opposed to a procedure like immunocytochemistry (ICC)?

Answer: In situ hybridization shows the presence of a specific mRNA for a protein. If a cell is synthesizing mRNA for a protein it usually means that the cell will also be making that protein. This method can be used to complement immunocytochemistry, or can be used if there is not a specific antibody available to directly measure the protein.

Textbook Reference: Multiple Neurobiological Techniques for Assessing the CNS 61. Name two human brain imaging techniques that give a static picture of the brain, and two techniques that can determine the amount of activity in different brain areas.

Answer: CAT and MRI scans give static pictures, whereas fMRI and PET scans measure brain activity.

Textbook Reference: Multiple Neurobiological Techniques for Assessing the CNS 62. Provide two examples of how genetic engineering has helped neuroscientists understand more about the role of genes, receptors, and peptides.

Answer: Transgenic mice have been used to create an animal model for Huntington’s disease. Testing treatments to relieve symptoms in these mice might lead to newer treatments for human patients, some of which may involve altering gene, receptor, or peptide functioning. Using knockout mice, researchers could determine the role of specific receptors in mediating drug-induced behaviors, for instance, what type(s) of dopamine receptors might be necessary for mediating locomotor stimulation produced by cocaine.

Textbook Reference: Multiple Neurobiological Techniques for Assessing the CNS

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Test Bank to accompany

Psychopharmacology, Third Edition Meyer • Quenzer

Chapter 5: Catecholamines Multiple Choice 1. Which of the following is not a catecholamine? a. Dopamine b. Glutamine c. Norepinephrine d. Epinephrine Answer: b Textbook Reference: Introduction 2. Increased levels of DA or NE in the nerve terminal decreases the rate of catecholamine synthesis by affecting the action of a. tyrosine hydroxylase. b. aromatic acid decarboxylase. c. dopamine β-hydroxylase. d. DOPA. Answer: a Textbook Reference: Catecholamine Synthesis, Release, and Inactivation 3. Which of the following most accurately represents the synthesis of the catecholamines? a. DOPA → tyrosine → dopamine → norepinephrine b. Tyrosine → DOPA → dopamine → norepinephrine c. Tyrosine → dopamine → DOPA → norepinephrine d. DOPA → dopamine → tyrosine → norepinephrine Answer: b Textbook Reference: Catecholamine Synthesis, Release, and Inactivation 4. Catecholamine levels can be decreased by , which serves to a. reserpine; block tyrosine hydroxylase b. α-methyl-para-tyrosine; inhibit uptake into vesicles c. α-methyl-para-tyrosine; block tyrosine hydroxylase d. Adderall; inhibit reuptake Answer: c Textbook Reference: Catecholamine Synthesis, Release, and Inactivation

.

5. Once synthesis has occurred, a protein called the is responsible for packaging molecules of dopamine into membrane packets for release.

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a. autoreceptor b. terminal receptor c. vesicular monoamine transporter d. dopamine transporter Answer: c Textbook Reference: Catecholamine Synthesis, Release, and Inactivation 6. A group of mice is given reserpine as part of an experiment. Behaviorally, these animals would be expected to show a. repetitive head and limb movements. b. sedation. c. stereotyped behaviors. d. increased activity.

Answer: b Textbook Reference: Catecholamine Synthesis, Release, and Inactivation 7. Activation of terminal autoreceptors inhibits dopamine release, in part, by a. increasing Cl– entry into the terminal. b. decreasing Ca2+ entry into the terminal. c. preventing reuptake into vesicles. d. decreasing Na+ entry into the terminal.

Answer: b Textbook Reference: Catecholamine Synthesis, Release, and Inactivation 8. Under conditions of high excitatory input, a dopamine neuron can switch from to , causing an increase in extracellular neurotransmitter levels. a. single-spiking mode; burst mode b. inhibitory; excitatory c. dopaminergic; adrenergic d. phasic; tonic Answer: a Textbook Reference: Catecholamine Synthesis, Release, and Inactivation 9. Signs of opioid withdrawal include increased heart rate, diarrhea, and elevated blood pressure, which can be relieved by stimulating a. µ opioid receptors. b. D2 autoreceptors. c. NE transporters. d. α2 autoreceptors.

Answer: d Textbook Reference: Catecholamine Synthesis, Release, and Inactivation 10. The first means of inactivation of the catecholamines is a. reuptake by transporter proteins. b. reuptake by autoreceptors. c. metabolism by monoamine oxidase.

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d. rapid diffusion.

Answer: a Textbook Reference: Catecholamine Synthesis, Release, and Inactivation 11. and exert their pharmacological effects by blocking monoamine reuptake. a. Cocaine; phenelzine b. Cocaine; tricyclic antidepressants c. Clonidine; tricyclic antidepressants d. Clonidine; yohimbine Answer: b Textbook Reference: Catecholamine Synthesis, Release, and Inactivation 12. The two most important enzymes in the metabolism of monoamines are a. catechol-O-methyltransferase and tyrosine hydroxylase. b. monoamine oxidase and homovanillic acid. c. catechol-O-methyltransferase and monoamine oxidase. d. monoamine oxidase and tyrosine hydroxylase.

Answer: c Textbook Reference: Catecholamine Synthesis, Release, and Inactivation 13. High levels of MHPG, HVA, and VMA in the blood and urine can indicate a. increased transporter activation. b. decreased catecholamine synthesis. c. dysfunctional receptors. d. increased catecholamine levels.

Answer: d Textbook Reference: Catecholamine Synthesis, Release, and Inactivation 14. The A9 and A10 cell groups are also known as the and the respectively. a. ventral tegmental area; locus coeruleus b. ventral tegmental area; substantia nigra c. substantia nigra; ventral tegmental area d. substantia nigra; locus coeruleus Answer: c Textbook Reference: Organization and Function of the Dopaminergic System

,

15. Dopaminergic cell bodies in the VTA send projections to the nucleus accumbens and the amygdala via the dopamine pathway. a. nigrostriatal b. mesocortical c. mesolimbic d. tuberohypophyseal Answer: c Textbook Reference: Organization and Function of the Dopaminergic System

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16. The dopamine pathway most important for regulating movement is the pathway. a. nigrostriatal b. mesocortical c. mesolimbic d. tuberohypophyseal Answer: a Textbook Reference: Organization and Function of the Dopaminergic System 17. 6-hydroxydopamine (6-OHDA) is a(n) _ used to . a. neurotoxin; damage catecholamine neurons b. antagonist; block catecholamine receptors c. transporter inhibitor; prevent catecholamine reuptake d. agonist; activate catecholamine receptors Answer: a Textbook Reference: Organization and Function of the Dopaminergic System 18. Which symptom would not be expected in an animal treated bilaterally with 6OHDA? a. Decreased interest in motivated behaviors such as eating and drinking b. Difficulty initiating movement c. Increased locomotor activity d. Sensory neglect Answer: c Textbook Reference: Organization and Function of the Dopaminergic System 19. To create a dopamine-deficient mouse that retains the ability to produce NE, the gene for is selectively restored in noradrenergic neurons. a. tyrosine hydroxylase b. 6-hydroxydopamine c. dopamine-beta-hydroxylase d. DOPA Answer: a Textbook Reference: Organization and Function of the Dopaminergic System 20. The major difference between D 1 and D 2 dopamine receptor subtypes is that one a. is ionotropic and the other is metabotropic. b. inhibits and the other stimulates adenylyl cyclase and cAMP. c. is found in the CNS and the other is found in the PNS. d. is very rare and the other is very common.

Answer: b Textbook Reference: Organization and Function of the Dopaminergic System 21. Which statement regarding D2 dopamine receptors is false? a. They are found only in the hypothalamus.

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b. They function as autoreceptors. c. They inhibit adenylyl cyclase and decrease the synthesis of cAMP. d. They can enhance K + channel opening via activation of a G protein.

Answer: a Textbook Reference: Organization and Function of the Dopaminergic System 22. A scientist investigating a newly identified receptor in rat cortex determines that it is a metabotropic receptor that regulates membrane-bound K + channels in some cells and inhibits adenylyl cyclase. Based on these findings, the receptor is most likely a(n) a. β-adrenergic receptor. b. D1 -like dopamine receptor. c. D2 -like dopamine receptor. d. autoreceptor.

Answer: c Textbook Reference: Organization and Function of the Dopaminergic System 23. Which statement regarding receptor up-regulation is false? a. It can lead to behavioral supersensitivity to an agonist. b. It can result from chronic treatment with an antagonist. c. It can result from depletion of normal neurotransmitter input. d. It happens only with autoreceptors.

Answer: d Textbook Reference: Organization and Function of the Dopaminergic System 24. Dopamine transporter knockout mice are hyperactive relative to wild -type mice because a. they produce more dopamine than wild-type mice. b. they have fewer receptors than wild-type mice. c. their dopaminergic neurons cannot remove dopamine from the synaptic cleft. d. they cannot synthesize dopamine.

Answer: c Textbook Reference: Organization and Function of the Dopaminergic System 25. Interpreting data from knockout mice can be complicated by the genetic strain of mouse used to create the mutation because a. some mouse strains do not breed well. b. strains vary widely in their behavior before any knockouts occur. c. some strains do not have the genes that the knockout is targeting. d. strains vary widely in their genetic makeup to begin with.

Answer: b Textbook Reference: Organization and Function of the Dopaminergic System 26. The main location of noradrenergic cell bodies in the CNS is the a. ventral tegmental area. b. locus coeruleus. c. substantia nigra.

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d. hypothalamus.

Answer: b Textbook Reference: Organization and Function of the Noradrenergic System 27. In the CNS, dopaminergic cell bodies are found primarily in the , while adrenergic cell bodies are found in the . a. midbrain; pons and medulla b. midbrain; hypothalamus c. pons and medulla; forebrain d. frontal cortex; cerebellum Answer: a Textbook Reference: Organization and Function of the Noradrenergic System 28. Which statement about norepinephrine is false? a. It acts in both the central nervous system and the autonomic nervous system. b. It is thought to play a role in arousal. c. NE terminals are found in widespread brain regions. d. NE producing cell bodies are widespread in the brain.

Answer: d Textbook Reference: Organization and Function of the Noradrenergic System 29. Why can norepinephrine be considered a hormone? a. It is released from the locus coeruleus into the general circulation. b. It is released from the hypothalamus into the general circulation. c. It is released from the adrenal glands into the general circulation. d. Actually, it cannot be considered a hormone, only a neurotransmitter.

Answer: c Textbook Reference: Organization and Function of the Noradrenergic System 30. Norepinephrine produced in cell bodies in the sympathetic chain ganglia a. enters the general circulation. b. can act on the heart and other organs. c. causes arousal by acting in the medulla. d. cannot cross the blood–brain barrier.

Answer: b Textbook Reference: Organization and Function of the Noradrenergic System 31. Noradrenergic receptors a. are ionotropic. b. inhibit adenylyl cyclase. c. are metabotropic. d. stimulate adenylyl cyclase.

Answer: c Textbook Reference: Organization and Function of the Noradrenergic System 32. 1 - and 2 -adrenoceptors

, while α2 -receptors

.

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a. stimulate adenylyl cyclase; enhance free Ca2+ levels b. inhibit adenylyl cyclase; stimulate adenylyl cyclase c. stimulate adenylyl cyclase; inhibit adenylyl cyclase d. increase K+ channel opening; inhibit adenylyl cyclase Answer: c Textbook Reference: Organization and Function of the Noradrenergic System 33. Injections of isoproterenol and phenylephrine into the lateral hypothalamus of the rat show that a. NE is involved in hunger. b. α1 - and β-receptors are involved in wakefulness. c. α1 - and β-receptors are involved in sedation. d. NE is important in pupil dilation.

Answer: b Textbook Reference: Organization and Function of the Noradrenergic System 34. Working memory can be enhanced by activation of in the PFC, while activation of in the PFC has detrimental effects on cognitive function. a. α1 -receptors; β1 -receptors b. α2 -receptors; α1 -receptors c. β2 -receptors; β1 -receptors d. α2 -receptors; β1 -receptors Answer: b Textbook Reference: Organization and Function of the Noradrenergic System 35. In the passive avoidance learning paradigm, learning is demonstrated by a. increased latency to enter the dark compartment. b. decreased latency to enter the dark compartment. c. increased physiological response to foot shock. d. increased latency to enter the light compartment.

Answer: a Textbook Reference: Organization and Function of the Noradrenergic System 36. Recent research investigating the effects of epinephrine on learning suggest that may improve cognitive function in aged individuals. a. decreasing NE levels b. increasing glucose levels c. decreasing vagus nerve activity d. increasing stress levels Answer: b Textbook Reference: Organization and Function of the Noradrenergic System 37. Why are adrenergic agonists and antagonists important in the treatment of many nonpsychiatric medical conditions? a. NE cells innervate many diverse brain regions. b. Movement disorders like Parkinson’s are caused by changes in NE systems.

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c. Alterations in brain NE can cause disorders of sleeping and eating. d. Adrenergic receptors are found on a wide variety of peripheral organs.

Answer: d Textbook Reference: Organization and Function of the Noradrenergic System because it .

38. The β2 -receptor agonist albuterol is used to treat a. asthma; constricts blood vessels in the bronchial lining and reduces congestion b. asthma; relaxes the bronchial muscles and creates a wider airway c. colds; constricts blood vessels in the nose and reduces congestion d. hypertension; decreases the rate of contraction of the heart Answer: b Textbook Reference: Organization and Function of the Noradrenergic System 39. The main reason for giving albuterol via inhaler is that it reduces a. congestion in the nose. b. cardiovascular side effects. c. the cost of the prescription. d. the time required for the drug to work.

Answer: d Textbook Reference: Organization and Function of the Noradrenergic System 40. In the treatment of hypertension, prazosin , while propranolol . a. blocks α1 -receptors and causes dilation of blood vessels; blocks β-receptors in the heart and decreases the contractile force b. blocks α1 -receptors and causes constriction of blood vessels; activates β receptors in the heart and increases the contractile force c. activates α1 -receptors and causes dilation of blood vessels; activates β-receptors in the heart and decreases the contractile force d. activates α1 -receptors and causes constriction of blood vessels; blocks β-receptors in the heart and increases the contractile force Answer: a Textbook Reference: Organization and Function of the Noradrenergic System 41. Hypertension and can be treated with β-receptor antagonists. a. depression b. drug addiction c. asthma d. anxiety Answer: d Textbook Reference: Organization and Function of the Noradrenergic System 42. Why might a physician prescribe metoprolol rather than propranolol to treat high blood pressure? a. It works only in the central nervous system. b. It is more effective because it acts as an antagonist at all adrenergic receptors. c. It dilates blood vessels by antagonizing α1 receptors.

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d. It has fewer side effects because it selectively antagonizes β1 -receptors.

Answer: d Textbook Reference: Organization and Function of the Noradrenergic System 43. β-receptor antagonists help patients with generalized anxiety by a. reducing some of the physical symptoms associated with anxiety. b. acting directly on brain regions involved in anxiety. c. increasing sympathetic nervous system activity, which makes the person feel better able to cope with anxiety-producing situations. d. causing sedation.

Answer: a Textbook Reference: Organization and Function of the Noradrenergic System

Matching 44. Match each numbered description with a lettered term below.

1. Lack of spontaneous movement 2. Antidepressant that inhibits monoamine oxidase 3. Drug used to treat Parkinson’s disease 4. Norepinephrine autoreceptors 5. Depletes catecholamines by inhibiting vesicular uptake 6. Antidepressant that selectively prevents NE reuptake 7. Receptors blocked by haloperidol a. α2 receptors b. Phenelzine c. Reboxetine d. Catalepsy e. L-DOPA f. Reserpine g. D2 receptors Answer: 1. d; 2. b; 3. e; 4. a; 5. f; 6. c; 7. g Textbook Reference: Catecholamine Synthesis, Release, and Inactivation

Short Answer/Essay 45. Describe the steps involved in the synthesis and metabolism of the catecholamines, including all the enzymes involved.

Answer: Synthesis: Tyrosine → tyrosine hydroxylase (TH) → DOPA → aromatic amino acid decarboxylase (AADC) → dopamine (D) → dopamine β-hydroxylase (DBH) → norepinephrine (NE).

Metabolism of dopamine and norepinephrine: Dopamine (D) → catechol-O-methyltransferase (COMT) and/or monoamine oxidase (MAO) → homovanillic acid (HVA).

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Norepinephrine (NE) → catechol-O-methyltransferase (COMT) and/or monoamine oxidase (MAO) → 3-methoxy-4-hydroxy-phenylglycol (MHPG) and vanillylmandelic acid (VMA).

Textbook Reference: Catecholamine Synthesis, Release, and Inactivation 46. Compare and contrast the function of autoreceptors and transporters.

Answer: Autoreceptors are found on the cell bodies, terminals, and dendrites of dopaminergic and noradrenergic neurons and inhibit neurotransmitter release when activated. Transporters are also found on axon terminals; they take neurotransmitter back up into the presynaptic neuron.

Textbook Reference: Catecholamine Synthesis, Release, and Inactivation 47. Describe the relationship between α2 -adrenergic receptors and opiate withdrawal, including pharmacological evidence supporting this relationship.

Answer: Opioid withdrawal symptoms include increased heart rate, diarrhea, and elevated blood pressure, all mediated by noradrenergic neurons in the peripheral nervous system.

Agonists at NE autoreceptors, which are α2 -receptors, inhibit the firing of these NE neurons and alleviate withdrawal symptoms. Administering α2 -receptor antagonists (which would block autoreceptors and increase NE activity) can elicit withdrawal symptoms in opioid-dependent patients, providing further evidence for a relationship between NE systems and opioid withdrawal.

Textbook Reference: Catecholamine Synthesis, Release, and Inactivation 48. Write a coherent and informative paragraph incorporating the following terms: phasic release, extracellular DA, tonic release, burst mode, VTA. Answer: Dopaminergic cells in the VTA have been shown to fire in two distinct patterns that have different consequences for extracellular DA levels in terminal regions. Tonic release of DA occurs during single-spike mode when the cell fires 4–5 spikes per second.

With increased excitatory input, the cell can switch to burst mode of 20 spikes per second. This results in the phasic release of DA in which extracellular levels of DA increase because it is being released faster than it can be cleared.

Textbook Reference: Catecholamine Synthesis, Release, and Inactivation 49. Describe the anatomy and briefly explain the function of the four main dopaminergic systems of the brain.

Answer: The four pathways are: • Nigrostriatal tract: Cell bodies in substantia nigra (A9) and terminals in dorsal striatum/caudate–putamen; involved in voluntary movement, motivational, and cognitive functions.

• Mesolimbic dopamine pathway: Cell bodies in ventral tegmental area (VTA; A10) and terminals in limbic structures, including nucleus accumbens, amygdala, septum and hippocampus; involved in reward/aversion and locomotor activation (behavioral arousal).

• Mesocortical dopamine pathway: Cell bodies in VTA and terminals in cerebral cortex, especially prefrontal cortex; involved in attention and working memory, implicated in schizophrenia.

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•

Tuberohypophyseal dopamine pathway: Cell bodies in hypothalamus and terminals in the pituitary gland; controls prolactin secretion from pituitary.

Textbook Reference: Organization and Function of the Dopaminergic System 50. Compare and contrast the D 1 and D2 receptors, including consequences of activation.

Answer: Both are metabotropic, G protein–coupled receptors. Both are found in the nucleus accumbens and dorsal striatum. Both are found postsynaptically and serve as heteroreceptors. D 2 receptors are also found presynaptically, acting as autoreceptors. D 1 receptors activate G s (a stimulatory G protein) when bound by DA or another D 1 agonist and stimulate adenylyl cyclase, increasing levels of the second messenger cAMP. In contrast, D 2 receptors inhibit adenylyl cyclase via G i (an inhibitory G protein) and decrease synthesis of cAMP. Some D 2 receptors enhance K + channel opening and thus hyperpolarize the cell membrane.

Textbook Reference: Organization and Function of the Dopaminergic System 51. Write a coherent and informative paragraph incorporating the following terms: behavioral supersensitivity, 6-OHDA, antagonist, receptor up-regulation, D 2 receptors.

Answer: Behavioral supersensitivity describes an increased reaction to D 2 agonists due, at least in part, to an up-regulation in D 2 receptors. This occurs after chronic D 2 antagonist treatment, 6-OHDA lesions, or other treatment that reduces D 2 receptor activation.

Textbook Reference: Organization and Function of the Dopaminergic System 52. Describe the evidence linking wakefulness to orexin and NE in the lateral hypothalamus.

Answer: Injections of α1 - and β-receptor agonists into the lateral hypothalamus increase the amount of time rats spend awake, especially when injected at the same time.

Stimulation of lateral hypothalamic orexin neurons also causes arousal, but not if the locus coeruleus is inhibited, indicating that orexin’s effects on arousal are mediated in part by NE. Textbook Reference: Organization and Function of the Noradrenergic System 53. Draw a curve describing the relationship between noradrenergic activity in the prefrontal cortex and working memory. Explain what this means, and describe the presumed receptor mechanisms responsible.

Answer: Students should draw an inverted U-shaped curve. This means that working memory is impaired when there is too little α2 -receptor activity, such as under sedated conditions, and when there is too much α1 -receptor activity, as occurs under stressful conditions.

Textbook Reference: Organization and Function of the Noradrenergic System 54. Describe two possible mechanisms by which peripheral administration of epinephrine could facilitate memory.

Answer: Epinephrine could activate β-receptors on the vagus nerve, which could then signal the locus coeruleus to release NE. Epinephrine could activate β-receptors in the liver, causing an increase in blood glucose, which easily crosses the blood–brain barrier and becomes fuel for the brain.

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Textbook Reference: Organization and Function of the Noradrenergic System

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Test Bank to accompany

Psychopharmacology, Third Edition Meyer • Quenzer

Chapter 6: Serotonin Multiple Choice 1. Another name for serotonin is a. 5-hydroxytryptophan. b. tryptophan. c. 5-hydroxytryptamine. d. tryptamine.

Answer: c Textbook Reference: Introduction 2. A specific marker for serotonin cells is a. tyrosine hydroxylase. b. tryptophan hydroxylase. c. AADC. d. MAO. Answer: b Textbook Reference: Serotonin Synthesis, Release, and Inactivation 3. What type of meal is most likely to increase brain levels of serotonin in animals? a. High carbohydrate, high protein b. High carbohydrate, low protein c. Low carbohydrate, low protein d. Low carbohydrate, high protein Answer: b Textbook Reference: Serotonin Synthesis, Release, and Inactivation 4. Why might increasing levels of tryptophan in the blood not increase brain serotonin levels? a. It doesn’t matter how much tryptophan is present, serotonin is made at a constant rate from brain stores of tryptophan. b. Tryptophan cannot cross the blood–brain barrier under any circumstances. c. Tryptophan competes with other amino acids for transport across the blood –brain barrier. d. Insulin is required for transport of tryptophan across the blood–brain barrier.

Answer: c Textbook Reference: Serotonin Synthesis, Release, and Inactivation 5. In order to study the effects of serotonin depletion in rodent studies,

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a. tryptophan hydroxylase is inhibited by injection of PCPA. b. tryptophan hydroxylase is stimulated by injection of PCPA. c. animals are fed a high carbohydrate, low protein diet. d. insulin is injected to alter the ratio of amino acids in the blood.

Answer: a Textbook Reference: Serotonin Synthesis, Release, and Inactivation 6. Researchers study the effects of serotonin depletion in human subjects by a. using the synthesis blocking drug PCPA. b. administering a special milkshake that is rich in tryptophan hydroxylase. c. injecting subjects with insulin to alter the ratio of amino acids in the blood. d. administering a cocktail of amino acids that compete with tryptophan for entry into the brain.

Answer: d Textbook Reference: Serotonin Synthesis, Release, and Inactivation 7. One potential consequence of administration of an amino acid cocktail to human subjects is that a. depressed subjects may experience a total remission of depressive symptoms if given a tryptophan-free cocktail. b. serotonin syndrome can result. c. previously healthy subjects can develop depression and anxiety if given a tryptophancontaining cocktail. d. previously depressed but currently recovered patients maintained on a 5 -HT-based antidepressant developed symptoms of depression if given a tryptophan-free cocktail.

Answer: d Textbook Reference: Serotonin Synthesis, Release, and Inactivation 8. All of the following can increase the presence of serotonin in the synaptic cleft except a. DOI. b. MDMA. c. fenfluramine. d. fluoxetine.

Answer: a Textbook Reference: Serotonin Synthesis, Release, and Inactivation 9. Autoreceptors on serotonin terminals are of the subtype, while somatodendritic autoreceptors are of the subtype. a. 5-HT1A; 5-HT3 b. 5-HT1A; 5-HT1B or 5-HT1D c. 5-HT1B or 5-HT1D; 5-HT1A d. 5-HT3 ; 5-HT1A Answer: c Textbook Reference: Serotonin Synthesis, Release, and Inactivation 10. The deactivation and metabolism of serotonin

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a. involves removal from the cleft by COMT. b. can be increased by SSRIs like Prozac. c. is selectively affected by the neurotoxin MDMA. d. yields the metabolite 5-HIAA. Answer: d Textbook Reference: Serotonin Synthesis, Release, and Inactivation 11. The principal acute action of MDMA is to a. prevent reuptake of serotonin. b. inhibit synthesis of serotonin. c. enhance tryptophan transport. d. enhance serotonin release.

Answer: d Textbook Reference: Serotonin Synthesis, Release, and Inactivation 12. MDMA was originally synthesized by the Merck pharmaceutical company as part of a project to find new substances that would a. reduce appetite. b. stop bleeding. c. reduce anxiety or nervousness. d. increase energy.

Answer: b Textbook Reference: Serotonin Synthesis, Release, and Inactivation 13. Which statement about MDMA is false? a. It produces an altered state of consciousness. b. It has been proposed as an adjunct to psychotherapy because it can enhance empathy. c. It has definitively been shown to produce degeneration of nerve fibers in all human users. d. It is considered a Schedule I substance according to the DEA. Answer: c Textbook Reference: Serotonin Synthesis, Release, and Inactivation 14. MDMA has recently been shown to improve the clinical response in patients undergoing treatment for a. PTSD. b. drug addiction. c. anexoria. d. depression.

Answer: a Textbook Reference: Serotonin Synthesis, Release, and Inactivation 15. Knockout mice lacking the serotonin transporter SERT exhibit all of the following except a. hypoactivity. b. a decrease in aggressiveness.

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c. enhanced maternal behavior. d. anxiety-like behavior.

Answer: c Textbook Reference: Serotonin Synthesis, Release, and Inactivation 16. The activity of serotonergic neurons in humans can be determined indirectly by measuring a. levels of 5-HIAA in cerebrospinal fluid. b. levels of 5-HIAA in blood. c. levels of 5-HT in cerebrospinal fluid. d. activation of SERT. Answer: a Textbook Reference: Serotonin Synthesis, Release, and Inactivation 17. Most of the cell bodies that produce serotonin in the CNS are found in the a. cerebellum. b. raphe nuclei. c. thalamus. d. limbic system.

Answer: b Textbook Reference: Organization and Function of the Serotonergic System 18. The fibers of serotonergic neurons are found a. mainly in the cerebellum and spinal cord. b. mainly in the midbrain, hypothalamus, and thalamus. c. mainly in the midbrain, pons, and medulla. d. in virtually all forebrain areas.

Answer: d Textbook Reference: Organization and Function of the Serotonergic System 19. Serotonergic neurons in the cat dorsal raphe nucleus stop firing during which behavioral state? a. REM sleep b. Active waking c. Slow-wave sleep d. Quiet waking Answer: a Textbook Reference: Organization and Function of the Serotonergic System 20. Pharmacologists have identified at least serotonin, most of which are . a. 14; ionotropic b. 7; ionotropic c. 7; metabotropic d. 14; metabotropic Answer: d

different receptor subtypes for

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Textbook Reference: Organization and Function of the Serotonergic System 21. All serotonin receptors are except for the receptor, which is . a. metabotropic; 5-HT5B; ionotropic b. metabotropic; 5-HT3 ; ionotropic c. ionotropic; 5-HT2C; metabotropic d. ionotropic; 5-HT1C; metabotropic Answer: b Textbook Reference: Organization and Function of the Serotonergic System 22. Which statement about 5-HT1A receptors is false? a. They serve as somatodendritic autoreceptors in the dorsal raphe nuclei. b. They are located postsynaptically in the forebrain. c. They serve as autoreceptors on serotonergic axon terminals in the forebrain. d. They are concentrated in the hippocampus, septal area, and parts of the amygdala.

Answer: c Textbook Reference: Organization and Function of the Serotonergic System 23. Activation of 5HT1A serotonin receptors can result in all of the following except a(n) a. increase in Na+ conductance across the cell membrane. b. reduction in cAMP synthesis. c. increase in K+ conductance. d. decrease in firing of the serotonergic neuron.

Answer: a Textbook Reference: Organization and Function of the Serotonergic System 24. Activation of 5HT1A serotonin receptors causes the neuronal membrane to be because _ channels are opened. + a. hyperpolarized; K b. depolarized; K+ c. hyperpolarized; Ca2+ d. depolarized; Na+ Answer: a Textbook Reference: Organization and Function of the Serotonergic System 25. Information regarding the effects of endogenous 5-HT on 5-HT1A receptors can be determined by administration of an antagonist such as a. busprione. b. 8-OH-DPAT. c. WAY 100635. d. ipsapirone.

Answer: c Textbook Reference: Organization and Function of the Serotonergic System

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receptors activate the phosphoinositide 26. Like α1 -adrenergic receptors, second-messenger system and thus increase intracellular levels. a. 5-HT2A; Ca2+ b. 5-HT1A; K+ c. 5-HT2A; cAMP d. 5-HT2A; Na+ Answer: a Textbook Reference: Organization and Function of the Serotonergic System 27. Which statement regarding the serotonin receptor family is true? a. 5-HT1A receptors are located primarily in the cerebral cortex. b. 5-HT2A receptors cause inhibition by decreasing adenyl cyclase and increasing potassium efflux. c. There is a family of five different 5-HT1 receptors. d. LSD and similar hallucinogens are most likely agonists at the 5-HT1A receptor.

Answer: c Textbook Reference: Organization and Function of the Serotonergic System 28. Drugs that act as agonists at 5-HT2A receptors produce a characteristic ―head-twitch‖ response in rodents and _ in humans. a. unwanted motor responses b. hallucinations c. Parkinsonian symptoms d. antischizophrenic effects Answer: b Textbook Reference: Organization and Function of the Serotonergic System 29. Later generation drugs used to treat schizophrenia, such as clozapine and risperidone, block/activate receptors and produce motor side effects. a. D2 ; severe b. 5-HT2A; fewer c. 5-HT2A; severe d. both D 2 and 5-HT2A; severe Answer: b Textbook Reference: Organization and Function of the Serotonergic System 30. Anti-migraine drugs known as triptans act as and cause of blood vessels. a. 5HT1A agonists; constriction b. 5-HT3 antagonists; dilation c. 5-HT1B/1D antagonists; constriction d. 5-HT1B/1D agonists; constriction Answer: d Textbook Reference: Organization and Function of the Serotonergic System 31. Which statement regarding 5-HT3 receptors is false?

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a. Some of them are located on peripheral terminals of the vagus nerve. b. Activation of these receptors inhibits the vomiting center in the brainstem. c. Drugs that block this receptor subtype are used to treat nausea in cancer chemotherapy patients. d. Ondansetron, granisetron, and palonosetron are all 5-HT3 receptor antagonists.

Answer: b Textbook Reference: Organization and Function of the Serotonergic System 32. 5,7-Dihydroxytryptamine (5,7-DHT) a. is a metabolite of serotonin. b. destroys the cell bodies of the serotonergic neurons. c. inhibits serotonin synthesis. d. must be administered directly into the brain.

Answer: d Textbook Reference: Organization and Function of the Serotonergic System 33. Which method(s) can be used to produce mice that lack brain serotonin throughout life, beginning with embryonic development? a. Administering the tryptophan hydroxylase inhibitor PCPA b. Knocking out the gene for tryptophan hydroxylase 2 c. Preventing the normal differentiation of cells that are destined to become serotonergic neurons d. Both b and c Answer: d Textbook Reference: Organization and Function of the Serotonergic System 34. In mice with a knockout of the tryptophan hydroxylase 2 gene, a. no serotonin can be synthesized in any part of the animal's body. b. no pharmacological treatment has been found that is able to restore serotonin, even temporarily. c. the circuitry of the serotonergic system (fiber innervation) is normal, despite the lack of serotonin. d. impulsive aggression is increased compared to wild-type mice.

Answer: d Textbook Reference: Organization and Function of the Serotonergic System 35. Which type of aggression is not observed in animals? a. Premeditated aggression b. Predatory aggression d. Maternal aggression d. Irritable aggression Answer: a Textbook Reference: Organization and Function of the Serotonergic System 36. One brain region implicated in the neural circuitry of aggression in rodents but not in humans is the

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a. amygdala. b. cingulate cortex. c. BNST. d. hypothalamus.

Answer: c Textbook Reference: Organization and Function of the Serotonergic System 37. Evidence supporting a link between low levels of 5-HT and/or receptor activation and increased aggression, or high levels of 5-HT and/or receptor activation and decreased aggression, comes from all of the following studies except for those a. measuring 5-HT release during play of violent video games. b. correlating 5-HIAA concentration in the cerebrospinal fluid and measures of aggressive behavior. c. using SSRIs to increase extracellular 5-HT levels. d. examining inhibition of tryptophan hydroxylase.

Answer: a Textbook Reference: Organization and Function of the Serotonergic System 38. Mice genetically engineered to lack central serotonin a. do not survive to birth. b. have difficulty with thermoregulation. c. demonstrate little to no aggressive behavior. d. breathe at a faster rate than wild-type mice.

Answer: b Textbook Reference: Organization and Function of the Serotonergic System 39. Evidence that serotonergic abnormalities may be involved in sudden infant death syndrome (SIDS) comes from studies showing that a. the incidence of SIDS decreases if infants are given SSRIs. b. response to a CO 2 challenge in mutant mice lacking central serotonin can be improved by treatment with DOI. c. apnea in mutant mice lacking central serotonin can be reversed with SSRIs. d. infants who died of SIDS had a reduced number of 5-HT2A receptors in their brain.

Answer: b Textbook Reference: Organization and Function of the Serotonergic System 40. Administration of is not likely to lead to a decrease in food intake and thus weight loss. a. 5-HT1B agonists b. 5-HT2C agonists c. 5-HT1A agonists d. 5-HT6 antagonists Answer: c Textbook Reference: Organization and Function of the Serotonergic System 41. Which statement regarding serotonin and anxiety is false?

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a. Buspirone is an effective antianxiety medication and a partial agonist at 5-HT1A receptors. b. Knockout mice lacking 5-HT1A receptors show increased anxiety on the elevated zero maze. c. Knockout mice lacking 5-HT2A receptors show decreased anxiety-like behaviors. d. The 5-HT2A/2C receptor agonist mCPP is an effective antianxiety medication.

Answer: d Textbook Reference: Organization and Function of the Serotonergic System 42. Studies using animal models have shown that serotonin is involved in a. cancer-related b. neuropathic c. hypoalgesia d. electric shock-induced Answer: b Textbook Reference: Organization and Function of the Serotonergic System

pain.

43. Administration of a 5-HT4 receptor partial agonist a. impairs memory consolidation in a 1-trial fear conditioning task. b. improves cognitive function in patients with Alzheimer’s disease. c. enhances learning and memory in various learning tasks in rodents and monkeys. d. affects cognitive function by inhibiting cholinergic transmission in the neocortex and hippocampus.

Answer: c Textbook Reference: Organization and Function of the Serotonergic System is being tested as a potential therapeutic agent to 44. The 5-HT6 antagonist improve cognitive function in patients with Alzheimer’s disease. a. idalopirdine b. donepezil c. vilazodone d. lorcaserin Answer: a Textbook Reference: Organization and Function of the Serotonergic System 45. In the gut, serotonin is synthesized by a. some neurons within the enteric nervous system. b. enterochromaffin cells. c. goblet cells. d. Both a and b Answer: d Textbook Reference: Organization and Function of the Serotonergic System 46. Serotonin release in the gut is stimulate by a. taking an SSRI. b. fasting.

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c. entry of food into the gut. d. Both a and c Answer: c Textbook Reference: Organization and Function of the Serotonergic System 47. One of the current treatments for irritable bowel syndrome (IBS) is alosetron, which acts as a a. 5-HT3 receptor antagonist. b. 5-HT6 recept or agonist. c. 5-HT4 receptor antagonist. d. 5-HT2 receptor agonist.

Answer: a Textbook Reference: Organization and Function of the Serotonergic System

Short Answer/Essay 48. Describe the synthesis of serotonin and explain why serotonin levels in the brain can be increased by consumption of a high-carbohydrate, low-protein meal.

Answer: Serotonin is synthesized from tryptophan in two steps: tryptophan to 5hydroxytryptophan (5-HTP), catalyzed by tryptophan hydroxylase; and 5-HTP to serotonin, catalyzed by aromatic amino acid decarboxylase. Serotonin levels in the brain can be increased by consuming a high-carbohydrate, low-protein meal because tryptophan competes with other large neutral amino acids for transport into the brain across the blood–brain barrier. Consumption of a high-carbohydrate, low-protein meal triggers insulin release, increases the ratio of plasma tryptophan to its competing amino acids, and thus increasing tryptophan entry into the brain.

Textbook Reference: Serotonin Synthesis, Release, and Inactivation 49. Explain the primary mechanism responsible for rapid termination of serotonergic transmission, and name an important class of drugs that acts on that mechanism.

Answer: Serotonergic transmission is rapidly terminated by reuptake by the 5-HT transporter. A major class of drugs acting on this mechanism are the selective serotonin reuptake inhibitors (SSRIs).

Textbook Reference: Serotonin Synthesis, Release, and Inactivation 50. Describe the primary acute mechanism of action of MDMA. What experimental evidence would you cite to convince someone not to take repeated high doses of MDMA (ecstasy)?

Answer: MDMA acutely releases serotonin from serotonergic neurons. Animal studies have shown that high doses of MDMA cause long-term reductions in brain serotonin levels and in serotonergic fiber staining. Long-term ecstasy exposure in humans has also been found to produce abnormalities in the serotonergic system and cognitive deficits.

Textbook Reference: Serotonin Synthesis, Release, and Inactivation

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51. Name the major serotonin cell clusters in the brain stem and describe their projection pathways.

Answer: The major serotonin cell clusters in the brain stem are the raphe nuclei, especially the dorsal and median raphe. These cells project to virtually all forebrain areas, including the neocortex, striatum, nucleus accumbens, thalamus, hypothalamus, and limbic system structures (hippocampus, amygdala, and septal area).

Textbook Reference: Organization and Function of the Serotonergic System 52. Describe the changes in dorsal raphe cell firing rate during different behavioral states in cats.

Answer: Firing is steady at a rate of 2 spikes per second during quiet waking. Firing is slightly increased during behavioral activity, greatly reduced during slow-wave sleep, and abolished during REM sleep.

Textbook Reference: Organization and Function of the Serotonergic System 53. Identify the two ways by which 5-HT1A receptors exert their postsynaptic effects. List two kinds of evidence supporting a role for 5-HT1A receptors in regulating anxiety.

Answer: 5-HT1A receptors inhibit adenylyl cyclase/reduce the rate of cAMP synthesis, and increase the opening of K + channels to cause membrane hyperpolarization. Evidence for regulating anxiety: The 5-HT1A partial agonist buspirone is used as an antianxiety medication, and 5-HT1A receptor knockout mice exhibit increased anxiety-like behavior in several standard behavioral tests.

Textbook Reference: Organization and Function of the Serotonergic System 54. How do 5-HT2A receptors exert their postsynaptic effects? Give an example of a 5HT2A receptor agonist and a 5-HT2A receptor antagonist.

Answer: 5-HT2A receptors activate the phosphoinositide second messenger system. DOI is an agonist; ketanserin and ritanserin are antagonists.

Textbook Reference: Organization and Function of the Serotonergic System 55. Explain what makes 5-HT3 receptors different from other serotonin receptors.

Identify one important therapeutic use of 5-HT3 receptor antagonists.

Answer: Unlike other serotonin receptors, 5-HT3 receptors are excitatory ionotropic receptors. 5-HT3 receptor antagonists are used therapeutically to counteract nausea and vomiting associated with cancer chemotherapy.

Textbook Reference: Organization and Function of the Serotonergic System 56. Describe the evidence linking serotonin and aggression in both humans and animal models. Give examples involving specific serotonin receptor subtypes.

Answer: Reduced cerebrospinal fluid concentrations of 5-HIAA have been linked to increased aggressiveness in patients with borderline personality disorder or more generally in people who exhibit antisocial behavior. In animal studies, aggressive behavior was decreased by administration of an SSRI, whereas aggressive behavior was increased by administration of a serotonin neurotoxin or a tryptophan hydroxylase inhibitor. Administration to rodents of either a 5-HT1A or a 5-HT1B receptor agonist reduces aggressive behavior, possibly due to the autoreceptor activity of these drugs.

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Textbook Reference: Organization and Function of the Serotonergic System 57. Explain how techniques of genetic engineering have contributed to our understanding of the behavioral and physiological functions of the serotonergic system.

Answer: Knockout mice have been generated in which key serotonergic genes such as the tryptophan hydroxylase gene, the serotonin transporter gene, or the genes for particular serotonergic receptors have been inactivated. By investigating the behavioral and/or physiological phenotypes produced by loss of a specific gene, researchers can infer the functional role(s) of the missing gene. In the case of the tryptophan hydroxylase2 (TPH2) gene, the effects of the knockout are due to a global loss of serotonin synthesis throughout the nervous system. In the case of the serotonin transporter gene, the effects of the knockout are due to a global increase in extracellular serotonin levels because of the loss of reuptake. In the case of specific receptor knockouts, the phenotype reflects the functional role of that serotonin receptor in behavioral and physiological regulation.

Textbook Reference: Organization and Function of the Serotonergic System 58. Imagine you are in charge of research and development of a pain medication program at a major pharmaceutical company. Assuming that you are targeting the serotonergic system in your drug development program, what pain model should you focus on? What kinds of changes in pain sensitivity have been associated with this pain model? List two different serotonergic receptors for which agonist drugs have been successful in alleviating pain in animal research.

Answer: The pain model to focus on is neuropathic pain, which has been associated with hyperalgesia and allodynia. Agonists at the 5-HT1A, 5-HT1B, 5-HT2C, and 5-H 7 have been shown to reduce models of neuropathic pain in animal studies.

Textbook Reference: Organization and Function of the Serotonergic System 59. Where does gut serotonin come from, what triggers its release, and what is its function?

Answer: Gut serotonin comes from neurons of the enteric nervous system and from enterochromaffin cells in the walls of the gut. Release of gut serotonin is triggered by ingestion of food. Serotonin functions to promote gut peristalsis and secretory activity.

Textbook Reference: Organization and Function of the Serotonergic System

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Test Bank to accompany

Psychopharmacology, Third Edition Meyer • Quenzer

Chapter 7: Acetylcholine Multiple Choice 1. Which statement about curare is false? a. It produces anesthesia. b. It produces paralysis and stops respiration. c. It is used on the tips of arrows by native tribes in South America. d. By taking it themselves, scientists determined that it does not reduce consciousness.

Answer: a Textbook Reference: Acetylcholine Synthesis, Release, and Inactivation 2. In acetylcholine synthesis, a. the key catalyzing enzyme is acetylcholinesterase. b. choline comes from the diet and the liver. c. acetyl coenzyme A limits synthesis, as it is not found in all cells. d. coenzyme A is an important precursor.

Answer: b Textbook Reference: Acetylcholine Synthesis, Release, and Inactivation 3. Acetylcholine neurons can be identified by the presence of a. acetylcholinesterase. b. acetyl coenzyme A. c. choline acetyltransferase. d. choline.

Answer: c Textbook Reference: Acetylcholine Synthesis, Release, and Inactivation 4. Manipulating acetylcholine synthesis with pharmacological agents a. is straightforward because of the pharmacological specificity of ChAT inhibitors. b. has led to significant clinical improvements in disorders like Alzheimer’s disease. c. may yield unfortunate side effects due to peripheral metabolism, such as a fishy odor. d. is straightforward because it relies entirely on the availability of precursors.

Answer: c Textbook Reference: Acetylcholine Synthesis, Release, and Inactivation 5. The drug vesamicol a. blocks acetylcholinesterase. b. decreases the amount of acetylcholine in the cytoplasm. c. increases the rate of choline acetyltransferase activity.

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d. decreases the release of acetylcholine from the terminal button.

Answer: d Textbook Reference: Acetylcholine Synthesis, Release, and Inactivation 6. Which of the following is the most severe toxin involving acetylcholine? a. Botulinum b. Prairie rattlesnake venom c. Hemicholinium-3 (HC-3) d. Black widow spider venom Answer: a Textbook Reference: Acetylcholine Synthesis, Release, and Inactivation 7. Black widow spider venom produces its effects by , while botulinum toxin causes its effects by . a. increasing metabolism of ACh; preventing release of ACh b. blocking ACh receptors in the PNS; blocking ACh receptors in the CNS c. preventing metabolism of ACh; increasing synthesis of ACh d. causing massive release of ACh; preventing release of ACh Answer: d Textbook Reference: Acetylcholine Synthesis, Release, and Inactivation 8. Botulinum toxin has been used for all of the following except a. cosmetic purposes (treatment of ―dynamic wrinkles‖). b. the treatment of facial and eyelid spasms. c. the treatment OCD and autism. d. the treatment of dystonias (prolonged muscle contractions).

Answer: c Textbook Reference: Acetylcholine Synthesis, Release, and Inactivation 9. Which statement regarding botulinum toxin is false? a. The bacterium grows anaerobically. b. It prevents fusion of the synaptic vesicle containing ACh with the presynaptic terminal. c. It is a mixture of seven related proteins. d. It is taken up by cholinergic neurons of the CNS. Answer: d Textbook Reference: Acetylcholine Synthesis, Release, and Inactivation 10. The function of AChE is to a. help transmission proceed smoothly at the neuromuscular junction. b. break acetylcholine into choline and acetic acid. c. metabolize excess acetylcholine in the terminal button. d. All of the above Answer: d Textbook Reference: Acetylcholine Synthesis, Release, and Inactivation

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11. Which of the following represents the correct order of events at the neuromuscular junction? a. AChE secreted by muscle cell → ACh metabolized into choline + acetic acid → choline transported back into terminal b. ACh metabolized into choline + acetic acid → AChE secreted by cholinergic neuron → choline transported back into terminal c. AChE secreted by muscle cell → ACh metabolized into choline + acetic acid → choline and acetic acid transported back into terminal d. Choline transported to neuromuscular junction → AChE secreted by muscle cell → ACh metabolized into choline + acetic acid Answer: a Textbook Reference: Acetylcholine Synthesis, Release, and Inactivation 12. The choline transporter can be blocked by a. vesamicol. b. hemicholinium-3. c. physostigmine. d. pyridostigmine.

Answer: b Textbook Reference: Acetylcholine Synthesis, Release, and Inactivation 13. Mutant mice lacking the choline transporter die within an hour or so of birth because they a. synthesize too much ACh. b. synthesize too little ACh. c. suffer from a buildup of acetic acid. d. cannot release ACh properly.

Answer: b Textbook Reference: Acetylcholine Synthesis, Release, and Inactivation 14. Which of the following is not an AChE inhibitor? a. HC-3 b. Neostigmine c. Sarin d. Insecticides Answer: a Textbook Reference: Acetylcholine Synthesis, Release, and Inactivation 15. Myasthenia gravis a. involves a low production of acetylcholine. b. is best treated by chemicals such as soman. c. involves an autoimmune process that destroys acetylcholine receptors. d. should be treated by neostigmine because it crosses the blood–brain barrier.

Answer: c Textbook Reference: Acetylcholine Synthesis, Release, and Inactivation

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16. The most important difference between pyridostigmine and sarin is that a. pyridostigmine is an irreversible AChE inhibitor; sarin is not. b. Sarin does not cross the blood–brain barrier; pyrodostigmine does. c. Sarin is an irreversible AChE inhibitor; pyrodostigmine is not. d. pyridostigmine is isolated from Calar beans; sarin is not.

Answer: c Textbook Reference: Acetylcholine Synthesis, Release, and Inactivation 17. Which agent is an irreversible AChE inhibitor? a. Physostigmine b. Neostigmine c. Vesamicol d. Soman Answer: d Textbook Reference: Acetylcholine Synthesis, Release, and Inactivation 18. was used during the Gulf War as a protective antidote to nerve gas. a. Pyridostigmine bromide b. Sarin c. Physostigmine bromide d. Soman Answer: a Textbook Reference: Acetylcholine Synthesis, Release, and Inactivation 19. Pyridostigmine can be used as an antidote to sarin because a. pyridostigmine acts on ACh release, not on its breakdown by AChE. b. temporary interactions between pyridostigmine and AChE prevent it from being permanently inactivated by sarin. c. pyridostigmine inactivates sarin by interacting with its ACh binding site. d. pyridostigmine prevents sarin from crossing the blood–brain barrier.

Answer: b Textbook Reference: Acetylcholine Synthesis, Release, and Inactivation 20. Acetylcholine is found in all of the following locations in the PNS except the a. neuromuscular junction. b. target organs of the sympathetic nervous system. c. target organs of the parasympathetic nervous system. d. sympathetic ganglion.

Answer: b Textbook Reference: Organization and Function of the Cholinergic System 21. Drugs like Cogentin and Artane would be given to someone with Parkinson’s disease because these drugs a. stimulate dopamine receptors. b. increase both acetylcholine and dopamine. c. prevent cell death in late stages of the disorder.

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d. decrease acetylcholine receptor activity and help restore a balance with dopamine.

Answer: d Textbook Reference: Organization and Function of the Cholinergic System 22. Which brain area(s) is/are not part of the basal forebrain cholinergic system (BFCS)? a. Diagonal band nuclei b. Substantia innominata c. Locus coeruleus d. Medial septal nucleus Answer: c Textbook Reference: Organization and Function of the Cholinergic System 23. Because cholinergic interneurons are clustered in the _, changes in cholinergic function can affect . a. striatum; movement b. thalamus; temperature regulation c. amygdala; emotional responses d. striatum; emotional responses Answer: a Textbook Reference: Organization and Function of the Cholinergic System 24. LDTg and PPTg cells a. are cholinergic interneurons. b. send cholinergic projections to many forebrain structures. c. utilize dopaminergic signals to control cholinergic cell function. d. send cholinergic projections to midbrain dopamine cell groups and to thalamic areas.

Answer: d Textbook Reference: Organization and Function of the Cholinergic System 25. Why have researchers been particularly interested in the agent 192 IgG-saporin? a. It is a new antidote for nerve gas exposure. b. It is a neurotoxin for cells in the brain stem cholinergic system. c. It destroys BFCS cells and causes cognitive deficits. d. It is a drug that might have use in the treatment of Alzheimer’s disease.

Answer: c Textbook Reference: Organization and Function of the Cholinergic System 26. Which statement about ACh and cognitive function is false? a. Atropine produces amnesic effects. b. Scopolamine produces amnesic effects. c. Acetylcholine release is inhibited in prefrontal cortex when animals are presented with a sensory stimulus. d. Alzheimer’s disease is associated with a loss of cholinergic neurons in the brain.

Answer: c Textbook Reference: Organization and Function of the Cholinergic System

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27. Nicotinic receptors a. are found on muscle cells at the neuromuscular junction. b. are metabotropic receptors. c. can be overly stimulated by the poison D-tubocurarine. d. possess two protein subunits, one α unit and one β unit.

Answer: a Textbook Reference: Organization and Function of the Cholinergic System 28. Which statement does not accurately describe activity at the nicotinic receptor? a. The channel opens rapidly and depolarization occurs. b. Sodium and/or calcium ions enter the next cell. c. Prolonged stimulation of receptors can lead to desensitization. d. Nicotinic receptors are only found on cell bodies and dendrites in the brain, not on nerve terminals.

Answer: d Textbook Reference: Organization and Function of the Cholinergic System 29. Activation of nicotinic receptors can increase release of neurotransmitter without affecting the firing rate of a neuron a. by allowing neurotransmitter to pass through the channel of the receptor. b. if the nicotinic receptors are located right on the presynaptic terminal of the neuron. c. only if the neuron in question has nicotinic receptors localized to its dendrites. d. only at the neuromuscular junction.

Answer: b Textbook Reference: Organization and Function of the Cholinergic System 30. Nicotinic receptors found on muscle cells require binding of molecules of ACh and are composed of subunits, a subunit, one γ, and either a δ or an ε subunit. a. two; two α; β1 b. five; two α; β2 c. two to five; two α1; β1 d. two; two α; β4 Answer: a Textbook Reference: Organization and Function of the Cholinergic System 31. With continuous exposure to , nicotinic receptors become a. antagonist; desensitized b. agonist; desensitized c. antagonist; resensitized d. agonist; blocked to depolarization Answer: b Textbook Reference: Organization and Function of the Cholinergic System

.

32. A drug that produces a depolarization block of muscle cells is a. muscarine.

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b. succinylcholine. c. nicotine. d. D-tubocurarine.

Answer: b Textbook Reference: Organization and Function of the Cholinergic System 33. Unlike , can readily cross the blood–brain barrier and thus have effects on the central nervous system. a. D-tubocurarine; mecamylamine b. atropine; succinylcholine c. mecamylamine; D-tubocurarine d. atropine; D-tubocurarine Answer: a Textbook Reference: Organization and Function of the Cholinergic System 34. Which statement regarding muscarinic receptors is false? a. They are metabotropic. b. They all inhibit the formation of cAMP. c. They can open potassium channels, causing inhibitory effects. d. They are widely distributed in the brain.

Answer: b Textbook Reference: Organization and Function of the Cholinergic System 35. Muscarinic receptors in the brain play a role in all of the following except a. motor function. b. cognition. c. tobacco smoking. d. dependence and addiction.

Answer: c Textbook Reference: Organization and Function of the Cholinergic System 36. An antagonist that selectively blocks M5 cholinergic receptors in the midbrain could potentially be used to treat a. diabetes. b. dry-mouth effect. c. drug dependence. d. heart disease.

Answer: c Textbook Reference: Organization and Function of the Cholinergic System 37. Stimulation of muscarinic receptors can decrease heart rate, while activation of peripheral M3 receptors can lead to an increase in . a. M5 ; heart rate b. M3 ; pupillary dilation c. M5 ; dry-mouth d. M2 ; insulin release

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Answer: d Textbook Reference: Organization and Function of the Cholinergic System 38. Ingestion of a parasympathomimetic agent, such as pilocarpine, can cause all of the following except a. sweating. b. pupillary dilation. c. salivation. d. diarrhea.

Answer: b Textbook Reference: Organization and Function of the Cholinergic System 39. Parasympatholytic agents a. have medical uses in ophthalmology and surgery. b. include atropine, which constricts the pupils. c. are rarely toxic, which is why they have been used throughout history. d. include pilocarpine and arecoline.

Answer: a Textbook Reference: Organization and Function of the Cholinergic System 40. Which drug/action pairings is incorrect? a. Vesamicol: inhibits vesicular uptake of ACh b. Atropine: muscarinic receptor antagonist c. Physostigmine: inhibits choline reuptake d. Sarin: irreversibly inhibits AChE Answer: c Textbook Reference: Organization and Function of the Cholinergic System

Short Answer/Essay 41. Describe the synthesis and breakdown of acetylcholine. Identify several beneficial and also harmful drugs that affect the metabolism of acetylcholine.

Answer: Acetylcholine is synthesized in the nerve terminal via the combination of choline and the acetyl group form acetyl coenzyme A, catalyzed by the enzyme choline acetyltransferase. Acetylcholine is metabolized by the enzyme acetylcholinesterase, which produces choline and acedic acid (acetate). Some diseases can benefit from inhibition of the metabolism of acetylcholine, and drugs such as neostigmine and pyridostigmine can inhibit the acetylcholinesterase and help relieve the symptoms of myasthenia gravis. However, irreversible inhibition of this enzyme with nerve gases used in warfare, such as sarin and soman, can be deadly due to desensitization of the nicotinic receptors of skeletal muscle at the diaphragm and subsequent respiratory paralysis.

Textbook Reference: Acetylcholine Synthesis, Release, and Inactivation

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42. Describe how storage and release of acetylcholine is affected by the following: vesamicol, black widow spider venom, and botulinum toxin. How is botulinum toxin being used in therapeutic and cosmetic settings today?

Answer: Vesamicol: blockade of acetylcholine uptake into synaptic vesicles. Black widow spider venom: initial release of acetylcholine, followed by diminished release.

Botulinum toxin: inhibition of acetylcholine release. Botulinum toxin can be used to decrease muscle spasms and can also be used to decrease wrinkles (used as Botox).

Textbook Reference: Acetylcholine Synthesis, Release, and Inactivation 43. Explain how a reversible AChE antagonist like pyridostigmine bromide can be used as an antidote of sorts against an irreversible AChE antagonist nerve gas such as sarin.

Answer: Pyridostigmine can occupy sites on AChE that will prevent sarin from gaining access to the enzyme. Then, because pyridostigmine is a reversible inhibitor, its effects will reverse. However, it is necessary for the pyridostigmine to be taken before exposure to sarin.

Textbook Reference: Acetylcholine Synthesis, Release, and Inactivation 44. Write an informative and coherent paragraph incorporating the following terms: myasthenia gravis, nicotinic receptor, neuromuscular junction, autoimmune disorder, neostigmine.

Answer: Myasthenia gravis is a neuromuscular junction autoimmune disorder in which antibodies are made against the nicotinic receptor. It is characterized by rapid muscle fatigue. It can be treated with inhibitors of acetylcholinesterase, which can prolong the life of acetylcholine in the synaptic cleft at the neuromuscular junction.

Textbook Reference: Acetylcholine Synthesis, Release, and Inactivation 45. Describe the distribution of acetylcholine neurons outside the central nervous system (i.e., in the periphery) and indicate which cholinergic receptors would be present postsynaptically in the various locations.

Answer: In the peripheral nervous system, all of the preganglionic neurons of the autonomic nervous system use ACh as a transmitter, and the postganglionic neurons contain nicotinic receptors at the ganglia, which respond to the ACh with excitation. At the tissue targets of the parasympathetic cholinergic neurons there are muscarinic receptors that respond to the released ACh. The cholinergic neurons leading to skeletal muscle (neuromuscular junctions) do not make a ganglionic connection, but rather go straight to the muscle and release ACh onto nicotinic receptors on the skeletal muscle.

Textbook Reference: Organization and Function of the Cholinergic System 46. Identify the cholinergic circuits in the central nervous system that are most important in cognitive functioning. Give one piece of evidence for your answer.

Answer: The basal forebrain cholinergic system (BFCS), which includes the nucleus basalis and medial septal nucleus, has been implicated with regard to cognitive functioning. One line of evidence in support of this idea is the finding that cholinergic neurotoxins, such as 192 IgG-saporin, can produce learning and/or attention deficits.

Textbook Reference: Organization and Function of the Cholinergic System

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47. Explain how 192 IgG-saporin works to create selective cholinergic lesions in the brain. Describe evidence suggesting that cortical ACh is important for attentional processing.

Answer: 192 IgG-saporin consists of two parts. One part is an antibody directed to bind to cholinergic neurons in the basal forebrain cholinergic system (BFCS). The other part, saporin, is a toxin. Because the toxin gets localized to the BFCS cholinergic neurons, it can be selective in the destruction that it causes. When animals are treated with the saporin complex, deficits in attentional processing can be observed, suggesting the importance of cortical ACh for attentional processing.

Textbook Reference: Organization and Function of the Cholinergic System 48. Describe the location and characteristics of nicotinic receptors. Name one drug that acts as an agonist and one drug that acts as an antagonist at these receptors.

Answer: Nicotinic receptors are found in the periphery in ganglia, where they receive the ACh input from the preganglionic neurons, and at the neuromuscular junction. They are ionotropic receptors that contain subunits, and they open up an ion channel for sodium ions when occupied by an agonist (such as ACh or nicotine). Examples of antagonists are mecamylamine and curare.

Textbook Reference: Organization and Function of the Cholinergic System 49. Describe the location of muscarinic receptors in the brain and periphery. List two central and two peripheral functions of these receptors. Finally, name a parasympathomimetic agent and a parasympatholytic agent.

Answer: Muscarinic receptors are found in the periphery on the target organs of the parasympathetic nervous system (heart, gut, etc.). Examples of brain location are basal forebrain cholinergic system (BFCS), neocortex, striatum, and hippocampus. In the brain, they may be involved in learning and memory, and in the reward response to psychoactive drugs. In the periphery, they are involved in slowing of the heart, and stimulating contraction of gut smooth muscle. A muscarinic parasympathomimetic agent (agonist) is muscarine, and a parasympatholytic agent (antagonist) is atropine.

Textbook Reference: Organization and Function of the Cholinergic System 50. Describe, in detail, the evidence supporting the assertion that muscarinic receptors may play a role in drug dependence and reward.

Answer: To measure rewarding properties of a drug, a place preference test can be performed. A rat or mouse can be trained to associate drug administration (such as morphine) with a particular side of a cage (rough surface, etc.), and to associate the other side of the cage (smooth surface, etc.) with just a saline administration. After repeated training, on the test day, the rat or mouse can be given the choice of going to either side of the cage. If the animal chooses to spend more time in the side associated with the morphine, this demonstrates a place preference for morphine, and is a property shared by psychoactive drugs that have the potential to become addictive drugs. Techniques have been developed that allow researchers to knock out a particular protein in an animal; usually a mouse is used for this purpose. When mice had their M5 muscarinic receptors

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knocked out, they did not show a place preference for morphine, suggesting a role of M5 muscarinic receptors in the rewarding effect of morphine.

Textbook Reference: Organization and Function of the Cholinergic System

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Test Bank to accompany

Psychopharmacology, Third Edition Meyer • Quenzer

Chapter 8: Glutamate and GABA Multiple Choice

1. Glutamate differs from other neurotransmitters such as acetylcholine (ACh), dopamine (DA), and serotonin (5HT) in that a. only specialized neurons in the brain synthesize and release glutamate. b. glutamate is the only neurotransmitter that causes EPSPs. c. glutamate also plays a role in protein synthesis and cell metabolism. d. glutamate can only be synthesized by a single chemical reaction.

Answer: c Textbook Reference: Glutamate Synthesis, Release, and Inactivation 2. VGLUT proteins a. are found in all cells containing glutamate. b. take up glutamate from the synaptic cleft. c. are identical to the plasma membrane transporters. d. come in three different forms that show little overlap in location.

Answer: d Textbook Reference: Glutamate Synthesis, Release, and Inactivation 3. Excitatory amino acid transporters (EAATs) a. may be defective in the disorder ALS or Lou Gehrig’s disease. b. are found on vesicle membranes in astrocytes and neurons. c. are found almost exclusively on neurons in the CNS. d. come in two different varieties, EAAT1 and EAAT2.

Answer: a Textbook Reference: Glutamate Synthesis, Release, and Inactivation 4. The findings from VGLUT knock out (KO) mice suggest that a. VGLUT2 expressing neurons are critical for survival. b. VGLUT2 expressing neurons have no impact on offspring survival. c. VGLUT1 and VGLUT2 KO are always found in the same neurons. d. VGLUT5 is important for the development of the auditory system.

Answer: a Textbook Reference: Glutamate Synthesis, Release, and Inactivation 5. Which statement about astrocytes is false? a. They contain glutamine synthetase.

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b. They remove glutamate from the extracellular fluid. c. They prevent excessive neuronal excitation and degeneration. d. They use the transporter EAAT3.

Answer: d Textbook Reference: Glutamate Synthesis, Release, and Inactivation 6. The presence of vesicular glutamate transporters and vesicular monoamine transporters in the same neurons suggests that a. cells that contain a lot of glutamate must store it in multiple types of vesicles. b. glutamate can be co-released as a neurotransmitter along with dopamine or serotonin. c. vesicular transporters are not selective. d. gene expression has gone wrong in these neurons.

Answer: b Textbook Reference: Glutamate Synthesis, Release, and Inactivation 7. Which statement about knockout mice lacking EAAT2 is false? a. They have a shortened life span. b. They develop spontaneous epileptic seizures. c. They are more susceptible to experimentally induced brain injury than wild-type mice. d. They exhibit normal weight gain throughout development.

Answer: d Textbook Reference: Glutamate Synthesis, Release, and Inactivation 8. Glutamate plays a specific functional role in a. synaptic plasticity. b. anxiety reduction. c. seizure suppression. d. the effects of benzodiazepines.

Answer: a Textbook Reference: Organization and Function of the Glutamatergic System 9. Why is it difficult to assign specific functional roles to glutamate, relative to other neurotransmitters? a. Because it is found throughout the brain b. Because it has very limited activity except in particular neural pathways c. Because its inhibitory action on the cortex makes it difficult to interpret d. Because it is not found in cortical neurons Answer: a Textbook Reference: Organization and Function of the Glutamatergic System 10. The AMPA receptor a. is metabotropic. b. handles most fast excitatory responses to glutamate. c. opens calcium channels when activated. d. is stimulated by the drug NBQX. Answer: b

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Textbook Reference: Organization and Function of the Glutamatergic System 11. The NMDA receptor a. selectively opens channels for sodium, but not calcium. b. is blocked by the antagonist NBQX. c. has only a single binding site. d. is responsive to both glutamate and glycine.

Answer: d Textbook Reference: Organization and Function of the Glutamatergic System 12. Which of the following is considered to be a glutamate co-agonist at the NMDA receptor site? a. Ketamine b. D-serine c. Magnesium d. Aspartate Answer: b Textbook Reference: Organization and Function of the Glutamatergic System 13. The NMDA receptor channel can be blocked by all of the following except a. Ca2+ ions. b. PCP. c. MK-801. d. ketamine.

Answer: a Textbook Reference: Organization and Function of the Glutamatergic System 14. Which event does not have to occur for NMDA receptor channel opening? a. An excitatory amino acid like glutamate must bind to the receptor. b. The PCP block must be removed. c. A co-agonist must bind at the glycine site. d. The membrane must be depolarized by some other receptor.

Answer: b Textbook Reference: Organization and Function of the Glutamatergic System 15. Drugs that work on the metabotropic glutamate receptor are of interest and under development for treating all of the following except a. depression. b. anxiety disorders. c. balance and vestibular problems. d. disorders with cognitive deficits.

Answer: c Textbook Reference: Organization and Function of the Glutamatergic System 16. Which statement about ampakines is false? a. They may reduce the rate of AMPA receptor desensitization.

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b. They enhance the action of glutamate at AMPA receptors. c. They replace glutamate at its binding site on the AMPA receptor. d. They improve performance in the DMS task.

Answer: c Textbook Reference: Organization and Function of the Glutamatergic System 17. In long-term potentiation, a. researchers apply a tetanic stimulus to the postsynaptic cell. b. changes that involve NMDA receptors occur in the induction phase. c. the expression phase involves kainate receptors. d. calcium inhibits the expression of additional AMPA receptors.

Answer: b Textbook Reference: Organization and Function of the Glutamatergic System 18. LTP is most often studied in a slice preparation from which area of the brain? a. Cerebral cortex b. Cerebellum c. Thalamus d. Hippocampus Answer: d Textbook Reference: Organization and Function of the Glutamatergic System 19. Which process does not occur in LTP? a. The AMPA-receptor mediated EPSP is facilitated. b. Calcium influx activates protein kinases. c. AMPA receptors increase in number and sensitivity. d. NMDA receptors are highly activated during the expression phase.

Answer: d Textbook Reference: Organization and Function of the Glutamatergic System 20. What evidence does not support the role of NMDA receptors in learning and memory? a. NMDA receptor antagonists disrupt the acquisition of spatial learning tasks. b. There are many NMDA receptors found in the hippocampus. c. CX717 enhances cognitive function. d. Doogie mice that overexpress the NR2B subunit show enhanced LTP. Answer: c Textbook Reference: Organization and Function of the Glutamatergic System 21. Chronic treatment with ampakine (CX929) to ―middle-age‖ rats a. increased their body weight by 25% relative to same aged controls. b. enhanced dendritic growth of their hippocampal CA1 neurons relative to same-aged controls. c. reduced the number of dendritic spines of hippocampal CA1 neurons relative to sameaged controls. d. had no effect on dendrites relative to controls.

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Answer: b Textbook Reference: Organization and Function of the Glutamatergic System 22. The excitotoxicity hypothesis states that a. repeated stimulation of neurons is the basis for learning and memory. b. tetanic stimulation of the presynaptic neuron can produce LTP in the recipient cell. c. overexposure to excitatory amino acid transmitters can result in depolarization and cell death. d. glutamate and aspartate play a critical role in the action of drugs like PCP. Answer: c Textbook Reference: Organization and Function of the Glutamatergic System 23. Cell death that occurs shortly after exposure to high concentrations of glutamate and other excitatory amino acids involves a. lysing and bursting of the cell. b. the breakup of DNA. c. shrinkage of the cell. d. phagocytosis.

Answer: a Textbook Reference: Organization and Function of the Glutamatergic System 24. Apoptosis a. begins with swelling of the cell. b. is a form of programmed cell death. c. involves lysing of the cell and disintegration into the extracellular space. d. typically indicates that a disease process has occurred.

Answer: b Textbook Reference: Organization and Function of the Glutamatergic System 25. Which statement about ischemia is false? a. It involves a massive decrease in glutamate release. b. It can result from a stroke or a heart attack. c. It involves disruption of blood flow and oxygen to tissue. d. It may be treated with glycine antagonists.

Answer: a Textbook Reference: Organization and Function of the Glutamatergic System 26. The best current treatment for amyotrophic lateral sclerosis (ALS) works on which neurotransmitter system (and thus suggests its’ involvement)? a. GABA b. Glutamate c. Dopamine d. Norepinephrine Answer: b Textbook Reference: Organization and Function of the Glutamatergic System

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27. Drugs that block GAT-1, such as Gabatril (tiagabine) are useful for treating a. memory disorders. b. ALS. c. seizure disorders. d. anxiety.

Answer: c Textbook Reference: GABA Synthesis, Release, and Inactivation 28. GABA metabolism a. takes place almost entirely in neurons. b. is undertaken by the enzyme GABA decarboxylase. c. is blocked by the drug GABA-T. d. can be inhibited by the antiseizure medication vigabatrin.

Answer: d Textbook Reference: GABA Synthesis, Release, and Inactivation 29. It has been suggested that abnormal firing of striatal GABAergic neurons may play a role in a. Alzheimer’s disease. b. amyotrophic lateral sclerosis. c. Parkinson’s disease. d. Down syndrome.

Answer: c Textbook Reference: Organization and Function of the GABAergic System 30. Which statement about GABA is false? a. It is found in many local interneurons. b. It is found in projection neurons carrying inhibitory information. c. It is found in Purkinje cells of the cerebellar cortex. d. It is found only in subcortical locations.

Answer: d Textbook Reference: Organization and Function of the GABAergic System 31. The GABA A receptor a. forms channels that permit chloride to move from the inside to the outside of the cell membrane. b. is composed of four subunits labeled α, β, γ, and δ. c. is a metabotropic receptor that inhibits cyclic AMP formation. d. is stimulated by the intoxicant drug muscimol.

Answer: d Textbook Reference: Organization and Function of the GABAergic System 32. The fly agaric mushroom produces all of the following effects except a. macroscopia. b. hypothermia. c. anorexia.

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d. hallucinations.

Answer: b Textbook Reference: Organization and Function of the GABAergic System 33. A drug sometimes used to induce seizures in laboratory animals is a. muscimol. b. muscarine. c. diazepam. d. picrotoxin.

Answer: d Textbook Reference: Organization and Function of the GABAergic System and the noncompetitive GABA A antagonist 34. The classic GABA A agonist both come from plants. a. muscimol; picrotoxin b. muscimol; pentylenetetrazol c. baclofen; picrotoxin d. bicuculline; baclofen Answer: a Textbook Reference: Organization and Function of the GABAergic System 35. Which drug(s) do(es) not enhance the effects of GABA on the GABA A receptor? a. Baclofen b. Ethanol c. Benzodiazepines d. Neurosteroids Answer: a Textbook Reference: Organization and Function of the GABAergic System 36. The α4 and α6 subunits make the GABA A receptor insensitive to a. barbiturates. b. neurosteroids. c. picrotoxin. d. benzodiazepines.

Answer: d Textbook Reference: Organization and Function of the GABAergic System 37. Benzodiazepine inverse agonist drugs would be a. anticonvulsant. b. anxiogenic. c. sedating. d. hypnotic.

Answer: b Textbook Reference: Organization and Function of the GABAergic System 38. Which characteristic do neurosteroids and benzodiazepines not share?

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a. They enhance GABA A receptor function. b. They have sedative-hypnotic effects. c. They bind to the BDZ site on the GABA A receptor. d. They act as local signaling molecules.

Answer: c Textbook Reference: Organization and Function of the GABAergic System 39. GABA B receptors a. cause potassium channel opening when stimulated. b. are ionotropic. c. are better studied than GABA A receptors. d. exert excitatory effects on cyclic AMP. Answer: a Textbook Reference: Organization and Function of the GABAergic System 40. GABA B receptors are unusual because a. they require glycine as a co-agonist. b. they are metabotropic but are composed of subunits. c. they simultaneously enhance Na+ channel opening and inhibit cAMP. d. they act as autoreceptors.

Answer: b Textbook Reference: Organization and Function of the GABAergic System 41. GABA B receptor agonists are clinically useful for treating a. anxiety. b. seizures. c. muscle spasms. d. alcoholism.

Answer: c Textbook Reference: Organization and Function of the GABAergic System

Short Answer/Essay 42. Describe the role of transporters and astrocytes in the clearance, metabolism, and synthesis of glutamate and GABA. Answer: After GLU is released, it is rapidly removed by GLU transporters. Different transporters then move the glutamate back into synaptic vesicles. These latter transporters are called excitatory amino acid transporters since they also can transport aspartate.

Astrocytes also have GLU transporters that may be region specific (cerebellum).

Astrocyte transporters also play a role in metabolism of GLU. Astrocytes take up GLU and covert a major portion of it to glutamine, which is then transported out of astrocytes and picked up by neurons, where it can be converted back into glutamate. There are also vesicular GABA transporters and transporters on both neurons and glia that remove GABA from the synapse. Astrocytes can metabolize GABA to form more GABA or glutamine (and thus glutamate).

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Textbook Reference: Glutamate Synthesis, Release, and Inactivation 43. Name the three ionotropic glutamate receptors in the brain. For each, identify the ions that move to create the depolarizing effects. What effect does the drug NBQX have on these receptors and on behavior?

Answer: AMPA and kainite depolarize mainly by Na+ entry; NMDA depolarizes by Na+ but also Ca2+ entry. NBQX can block AMPA and kainite receptors but not NMDA. Exposure to high doses of NBQX causes sedation, hypoactivity, and balance problems.

Textbook Reference: Organization and Function of the Glutamatergic System 44. Explain how the coincidence detection feature of NMDA receptors may allow them to play a role in associative learning.

Answer: The NMDA receptor channel only opens when two events occur close together—glutamate is released onto the NMDA receptor (assuming glycine is also bound to its site), and the cell membrane is already depolarized by stimulation of a different excitatory receptor. Associative learning involves the close pairing of two stimuli, and repeated pairing of the ―neutral‖ stimulus with an unconditioned stimulus results in a strong connection. This simple type of learning is argued to be similar to what happens with NMDA receptors during learning.

Textbook Reference: Organization and Function of the Glutamatergic System 45. Describe the role of NMDA and AMPA receptors in the induction and expression phases of long-term potentiation (LTP).

Answer: During the induction of LTP, a tetanic stimulus is activated which results in significant glutamate release, which causes prolonged activation of AMPA receptors (and greater postsynaptic depolarization). This allows Mg 2+ ions to dissociate from the NMDA receptor channels and Ca2+ to enter the cell through these channels. Ca2+ ions can then act as second messengers, resulting in an alteration in the postsynaptic cell that can result in an enhanced EPSP (LTP). NMDA receptors play a critical role in the induction phase but not the expression phase. AMPA receptors are necessary for LTP expression since it is an AMPA receptor-mediated EPSP that is facilitated in LTP. Textbook Reference: Organization and Function of the Glutamatergic System 46. Briefly describe how data from a mouse model of amyotrophic lateral sclerosis (ALS) supports the role of the glutamate system.

Answer: ALS is a fatal disease that involves a slow but progressive degeneration of motor neurons in the spinal cord and cortex. Glutamate-induced excitotoxicity has been proposed as one potential mechanism and while there is not conclusive evidence yet in human studies, there is a mouse model of ALS. Administration of a drug that enhances EAAT2 (excitatory amino acid transporter 2) expression caused a significantly slower loss of motor function and prolonged life span in the mouse model. EAAT2 is critically important for glutamate clearance by astrocytes and so there is less glutamate available for overexcitation.

Textbook Reference: Organization and Function of the Glutamatergic System

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47. Distinguish between short-term excitotoxic effects of glutamate and the delayed type of programmed cell death that occurs in adult animals.

Answer: Prolonged stimulation of glutamate receptors can cause cell death within just a few hours. This type of cell death is necrosis—it is characterized by lysis (bursting) of the cell due to osmotic swelling and other injurious consequences due to prolonged glutamate stimulation. Additionally, there are slower programmed forms of cell death that either have some of the features of necrosis or are mediated by apoptosis, which involves disruption of the cell nucleus and breakdown of DNA.known as programmed cell death.

Textbook Reference: Organization and Function of the Glutamatergic System 48. Describe the processes by which GABA is inactivated and metabolized. Identify two drugs that affect these processes, and indicate what effect they have on behavior.

Answer: GABA is removed from the synapse by transporters on neurons and on glia.

There have been three transporters identified but GAT-1 has received considerable attention because there is a drug, tiagabine, which blocks this transporter. This results in increased GABA in the synapse and is used as an adjunctive therapy for individuals with partial seizures that are resistant to treatment. GABA breakdown occurs through several steps, beginning with the enzyme GABA aminotransferase (GABA-T) and leading to final product, succinate. This enzyme is found in both GABA neurons and astrocytes.

Vigabatrin is an irreversible inhibitor of GABA-T. Administration of this drug results in increased GABA levels and has anticonvulsant effects.

Textbook Reference: GABA Synthesis, Release, and Inactivation 49. Characterize the GABA A receptor complex in terms of its subunits, ion channel, and the additional binding sites.

Answer: GABA A receptors are ion channels that permit Cl– ions to enter the postysynaptic cell, resulting in membrane hyperpolarization. The GABA A has 5 subunits.

Three or four different kinds of subunits may be found within a particular GABA A receptor. These different kinds of subunits are designated by the Greek letters α, β, γ, and δ. Most GABA A receptors are thought to contain two α subunits, two β, and one δ. A number of drugs interact with sites on the GABA A receptor that are distinct from GABA, including binding sites for BDZ, barbiturates, and neurosteroids, as well as a negative modulatory site for picrotoxin and related convulsant drugs.

Textbook Reference: GABA Synthesis, Release, and Inactivation 50. Name one GABA A receptor agonist and two antagonists, and compare their effects on behavior.

Answer: Muscimol is a classic GABA A that comes from mushrooms. It can cause hallucinations and a type of intoxication that includes elevation of mood, difficulty concentrating, ataxia, catalepsy, and hyperthermia. Bicuculine is a competitive antagonist for GABA A. It has potent convulsant effects. Picrotoxin, which comes from the seeds of an East Indian shrub, is another example of a GABA A antagonist and it also can produce seizures.

Textbook Reference: Organization and Function of the GABAergic System

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51. What are benzodiazepines and how do they affect GABA? Why might a doctor or psychiatrist prescribe benzodiazepines?

Answer: Benzodiazepenes (BDZs) are anxiolytics and their main mechanism of action is through positive allosteric modulation of the GABA A receptor; thus it enhances GABAmediated synaptic inhibition. BDZs have been used to reduce anxiety.

Textbook Reference: Organization and Function of the GABAergic System 52. Explain how the GABA B receptor is structurally and functionally different from the GABA A receptor.

Answer: The GABA B receptor requires two different subunits in order to assemble in the membrane. These receptors are located both postsynaptically and presynaptically. The postsynaptic receptors inhibit neuronal firing through stimulation of K + channel opening.

Presynaptic GABA B receptors are found on axon terminals of GABAergic neurons (autoreceptors) and on some terminals of cells using a different neurotransmitter such as glutamate. These presynaptic receptors reduce neurotransmitter release from the nerve terminal by inhibiting Ca2+ channel opening. Both post- and presynaptic GABA B receptors also inhibit adenylyl cyclase, thereby reducing the rate of cAMP formation.

GABA B has been implicated in a number of behavioral functions including learning and memory, anxiety and depression-like behaviors, and responses to drugs of abuse.

Textbook Reference: Organization and Function of the GABAergic System

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Test Bank to accompany

Psychopharmacology, Third Edition Meyer • Quenzer

Chapter 9: Drug Abuse and Addiction Multiple Choice 1. According to the 2016 National Survey on Drug Use and Health, 137 million Americans and more than 63 million Americans . a. smoked marijuana; drank alcohol b. drank alcohol; used tobacco c. drank alcohol; used cocaine or heroin d. used tobacco; used one or more illicit drugs Answer: b Textbook Reference: Introduction to Drug Abuse and Addiction 2. In the United States, the most commonly used illicit drug is a. marijuana. b. heroin. c. cocaine. d. oxycontin.

Answer: a Textbook Reference: Introduction to Drug Abuse and Addiction 3. Most illicit drug users are in the year-old age range. a. 12 or older b. 12-17 c. 18-25 d. 26 or older Answer: c Textbook Reference: Introduction to Drug Abuse and Addiction 4. The development of in 1858 contributed to the development of ―soldier’s disease,‖ or opiate addiction during the Civil War. a. cough syrup with codeine b. Vin Mariani (wine fortified with cocaine) c. the hypodermic syringe d. the temperance movement Answer: c Textbook Reference: Introduction to Drug Abuse and Addiction 5. In 1914, the passage of the cocaine.

regulated use and dispensing of opioid drugs and

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a. Pure Food and Drug Act b. Harrison Act c. Marijuana Tax Act d. Controlled Substances Act Answer: b Textbook Reference: Introduction to Drug Abuse and Addiction 6. The Controlled Substances Act created _ and established _ of controlled substances. One highly addictive substance not covered by this legislation is . a. a prohibition law; penalties for possession; nicotine b. the Drug Enforcement Agency; penalties for possession; alcohol c. a tax on narcotics and marijuana; five schedules; nicotine d. the Drug Enforcement Agency; five schedules; alcohol Answer: d Textbook Reference: Introduction to Drug Abuse and Addiction 7. Which drug is not found in nature? a. Nicotine b. THC c. Amphetamine d. Cocaine Answer: c Textbook Reference: Introduction to Drug Abuse and Addiction 8. Because of early theories equating addiction with , the drug thought to be an addictive substance. a. euphoria; cocaine b. physical dependence; cocaine c. physical dependence; morphine d. euphoria; morphine Answer: b Textbook Reference: Introduction to Drug Abuse and Addiction 9. Two primary features of the contemporary idea of addiction are a. craving; substance abuse b. physical dependence; relapse c. craving; relapse d. withdrawal; relapse Answer: c Textbook Reference: Introduction to Drug Abuse and Addiction

was not

_ and

.

10. The DSM-5 groups ten designated classes of drugs into a group called ―substancerelated disorders.‖ What is the rationale for this grouping? a. Although these drugs all have very different circuitry, they also share abuse potential. b. These drugs all share the ability to activate the neural circuitry that mediates ―reward.‖ c. These drugs all can produce a strong physical dependence and withdrawal.

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d. Studies have shown that addiction to these drugs is always fatal.

Answer: b Textbook Reference: Introduction to Drug Abuse and Addiction 11. In the DSM-5, is included in the non-substance-related addiction category. a. internet addiction b. binge eating c. sex addiction d. pathological gambling Answer: d Textbook Reference: Introduction to Drug Abuse and Addiction 12. Which of the following is not necessarily a part of the cycle of pathological drug use that can lead to addiction? a. Preoccupation with drug and anticipation of use b. Periods of intoxication and/or bingeing on the drug c. Periods of relatively prolonged abstinence from the drug d. Periods of withdrawal and negative affect Answer: c Textbook Reference: Introduction to Drug Abuse and Addiction 13. According to the Schedule of Controlled Substances, substances considered Schedule II a. include compounds that have medicinal value and no abuse potential b. have high abuse potential with severe dependence liability. c. have no accepted medical use in the United States and have high abuse potential. d. include compounds containing limited quantities of certain narcotics or nonnarcotic drugs.

Answer: b Textbook Reference: Features of Drug Abuse and Addiction 14. In general, the is positively correlated with . a. ability of a substance to cause relapse; its duration of action b. addiction potential of a substance; its speed of onset c. duration of action of a substance; its speed of onset d. speed of onset of a substance; its ability to cause relapse Answer: b Textbook Reference: Factors That Influence the Development and Maintenance of Drug Abuse and Addiction 15. Which statement about drug self-administration procedures is false? a. They rely on positive reinforcement produced by the substance being investigated. b. The typical dose–response function is an inverted U-shaped curve. c. Antidepressants and antipsychotics are readily self-administered by animals. d. In general, the reinforcing properties of an addictive drug increase as the dose is increased, within a certain range.

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Answer: c Textbook Reference: Factors That Influence the Development and Maintenance of Drug Abuse and Addiction 16. The relative strength of drug reinforcement can be measured using a schedule of drug self-administration. a. fixed-ratio b. variable-ratio c. progressive-ratio d. progressive-interval Answer: c Textbook Reference: Factors That Influence the Development and Maintenance of Drug Abuse and Addiction 17. In a progressive-ratio procedure, the response requirement at which an animal stops responding for drug is called the point. a. saturation b. breaking c. quitting d. intoxication Answer: b Textbook Reference: Factors That Influence the Development and Maintenance of Drug Abuse and Addiction 18. In general, drugs of abuse the threshold for rewarding brain stimulation. a. decrease b. increase c. do not affect d. first increase, then decrease Answer: a Textbook Reference: Factors That Influence the Development and Maintenance of Drug Abuse and Addiction 19. The increase in threshold for electrical self-stimulation of the brain produced by withdrawal from chronic treatment with drugs of abuse is generally interpreted to indicate a(n) a. state of intoxication. b. increase in sensitivity of the reward circuit. c. state of craving. d. decrease in sensitivity of the reward circuit.

Answer: d Textbook Reference: Factors That Influence the Development and Maintenance of Drug Abuse and Addiction 20. Through classical conditioning, environmental stimuli associated with cause relapse via _.

can

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a. withdrawal states; conditioned withdrawal and craving b. drug use; conditioned responding and physical dependence c. physical dependence; unconditioned responding and craving d. abstinence; unconditioned withdrawal Answer: a Textbook Reference: Factors That Influence the Development and Maintenance of Drug Abuse and Addiction 21. Malcolm et al. (2016) showed that regional brain activation after viewing methamphetamine stimuli (versus neutral visual stimuli) was a. greater in the hippocampus and periaqueductal gray in people diagnosed with methamphetamine dependence, relative to controls. b. greater in the ventral striatum and medial frontal cortex in people diagnosed with methamphetamine dependence, relative to controls. c. reduced in the ventral striatum and medial frontal cortex in people diagnosed with methamphetamine dependence, relative to controls. d. reduced in the hippocampus and periaqueductal gray in people diagnosed with methamphetamine dependence, relative to controls.

Answer: b Textbook Reference: Factors That Influence the Development and Maintenance of Drug Abuse and Addiction 22. The drug discrimination paradigm can be used to determine all of the following except a. whether an animal can readily discriminate a drug from a vehicle or saline. b. whether the effects of one drug ―generalize‖ to that of another. c. how hard an animal is willing to work for a drug. d. ―dose equivalents‖ of different drugs that can produce a similar internal state.

Answer: c Textbook Reference: Factors That Influence the Development and Maintenance of Drug Abuse and Addiction 23. Which statement about addiction and genetics is true? a. If both parents are alcoholics/drug addicts, their offspring will also be alcoholics/drug addicts, but if only one parent is affected, any offspring has a 50% chance of developing a problem. b. The addiction gene has been identified. c. A large number of genes influence susceptibility to addiction. d. If drug or alcohol problem do not run in a family, other family members will not develop a problem either.

Answer: c Textbook Reference: Factors That Influence the Development and Maintenance of Drug Abuse and Addiction

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24. Suppose Robert is trying to stop drinking alcohol, but his anxiety levels increase dramatically when he stops. If he increases his alcohol consumption to cope with this anxiety, his behavior could most readily be explained by the a. self-medication hypothesis. b. conclusion that his anxiety and his alcohol problem come from some shared factors. c. conclusion that one or more of his family members must also have an alcohol problem. d. conclusion that he must be under a great deal of stress.

Answer: a Textbook Reference: Factors That Influence the Development and Maintenance of Drug Abuse and Addiction 25. According to the self-medication hypothesis, individuals suffering from anxiety should prefer , and those suffering from depression should prefer . a. cocaine; alcohol b. cocaine; heroin c. alcohol; cocaine d. alcohol; heroin Answer: c Textbook Reference: Factors That Influence the Development and Maintenance of Drug Abuse and Addiction 26. A comprehensive model of drug addiction could be considered a model. a. disease b. medical c. biopsychosocial d. moral Answer: c Textbook Reference: Factors That Influence the Development and Maintenance of Drug Abuse and Addiction 27. Genome-wide associated studies (GWAS) look at the potential role of genetics in drug addiction by a. focusing on the potential involvement of genes that are selected based on the biochemical mechanism or mechanisms that underlie addiction. b. looking for chromosomal regions that tend to associate with addiction, and for mutations. c. investigating the entire genome in search of alleles that associate with addiction. d. All of the above Answer: c Textbook Reference: Factors That Influence the Development and Maintenance of Drug Abuse and Addiction 28. The proposed reward circuit involved in the rewarding and reinforcing effects of abused drugs incorporates many neuroanatomical structures but does not include the a. amygdala. b. cerebellum.

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c. nucleus accumbens. d. ventral pallidum.

Answer: b Textbook Reference: The Neurobiology of Drug Addiction 29. The extended amygdala includes all of the following except for the a. shell of the nucleus accumbens. b. central nucleus of the amygdala. c. bed nucleus of the stria terminalis. d. ventral tegmental area.

Answer: d Textbook Reference: The Neurobiology of Drug Addiction 30. Dopaminergic activity in the mesolimbic dopamine pathway is essential for drug reward in the case of but not in the case of . a. cocaine; heroin b. heroin; alcohol c. amphetamine; cocaine d. alcohol; heroin Answer: a Textbook Reference: The Neurobiology of Drug Addiction 31. The concept of incentive–sensitization distinguishes between a. drug seeking; drug taking b. drug liking; drug wanting c. drug liking; drug taking d. craving; drug seeking Answer: b Textbook Reference: The Neurobiology of Drug Addiction

and

.

32. Which of the following does not fit with the addiction-related neuroadaptations proposed by Koob and LeMoal? a. As drug users become dependent, less dopamine is released in the nucleus accumbens. b. Early recreational drug use is accompanied by increased dopamine and opioid activity. c. Increased norepinephrine and CRF play a role in recreational drug use. d. CRF levels in the amygdala increase as drug users become dependent.

Answer: c Textbook Reference: The Neurobiology of Drug Addiction 33. According to the opponent-process model of addiction, drug dependence causes to be shifted downward, through a process of . a. the hedonic set-point; sensitization b. the hedonic set-point; allostasis c. allostasis; tolerance d. allosatsis; sensitization Answer: b

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Textbook Reference: The Neurobiology of Drug Addiction 34. In addition to important changes in the dopamine system, from the appears to be involved in the transition to habitual, compulsive drug-seeking in animal models. a. serotonin; prefrontal cortex b. serotonin; nucleus accumbens c. glutamate; prefrontal cortex d. glutamate; amygdala Answer: c Textbook Reference: The Neurobiology of Drug Addiction 35. The transcription factor FosB a. is rapidly induced after administration of many drugs of abuse. b. accumulates in cells of the amygdala. c. up-regulates expression of all genes it affects. d. exhibits tolerance with repeated drug exposures.

Answer: a Textbook Reference: The Neurobiology of Drug Addiction 36. Which statement about mice genetically engineered to overexpress FosB in the dorsal striatum and nucleus accumbens relative to wild-type mice is false? a. They develop a conditioned place preference for cocaine and morphine at lower doses. b. They show an increased locomotor response to cocaine. c. They show a greater reduction in anxiety in response to alcohol. d. They do not develop physical dependence, withdrawal, or tolerance to morphine.

Answer: d Textbook Reference: The Neurobiology of Drug Addiction 37. Which of the following best represents the involvement of epigenetics in the progression to addiction? a. Environmental stimuli → acute drug exposure → repeated drug exposure/addiction → modified gene expression → epigenetic changes b. Environmental stimuli → acute drug exposure → epigenetic changes → modified gene expression → repeated drug exposure/addiction c. Environmental stimuli → modified gene expression → acute drug exposure → repeated drug exposure/addiction → epigenetic changes d. Acute drug exposure → environmental stimuli → modified gene expression → epigenetic changes → repeated drug exposure/addiction Answer: b Textbook Reference: The Neurobiology of Drug Addiction 38. According to the incentive sensitization theory of addiction, as a person develops a drug addiction, the user experiences an increase in , with no change or even a decrease in . a. drug liking; drug wanting

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b. drug wanting; drug liking c. drug reward; drug craving d. positive reinforcement; negative reinforcement Answer: b Textbook Reference: The Neurobiology of Drug Addiction 39. The model of addiction is based on the idea that brain dysfunction occurs as a result of repeated drug exposure. a. opponent–process b. susceptibility c. moral d. disease Answer: d Textbook Reference: The Neurobiology of Drug Addiction

Matching 40. Match each numbered description with a lettered term below.

1. Changes in the brain resulting from repeated drug use 2. Attention-getting and desirable properties of stimuli 3. Substance considered Schedule I 4. Supports drug taking by decreasing withdrawal symptoms 5. Unpleasant mood state 6. Substance considered Schedule II 7. Psychiatric disorder(s) in addition to addiction a. Negative reinforcement b. Dysphoria c. Neuroadaptation d. Marijuana e. Comorbidity f. Incentive salience g. Cocaine Answer: 1. c; 2. f; 3. d; 4. a; 5. b; 6. g; 7. e Textbook Reference: Features of Drug Abuse and Addiction

Short Answer/Essay 41. Identify the major pieces of federal drug legislation and the purpose of each. What effect did these laws have on drug use in the United States?

Answer: The Pure Food and Drug Act of 1906 regulated labeling of patent medicines and created the FDA. The Harrison Act of 1914 regulated dispensing and use of opioid drugs and cocaine. Prohibition banned alcohol sales except for medicinal use in 1920. The Marijuana Tax Act of 1937 banned nonmedical use of cannabis. And the Controlled

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Substances Act established the schedule of controlled substances and created the DEA in 1970.

Textbook Reference: Introduction to Drug Abuse and Addiction 42. Describe three procedures researchers can use to measure whether drugs have rewarding effects in animal models.

Answer: Self-administration—will the animal voluntarily press a lever or poke their nose in a hole in order to receive a small amount of drug infused directly into their bloodstream. Progressive-ratio—this uses self-administration but provides useful information regarding the relative strength of drug reinforcement. The animal is trained to push a lever for a low dose of drug and once this is learned, the schedule involves increasing the number of presses required for a single drug administration. The response rate at which the animal stops pressing the bar is called the break point. Place conditioning—animals are trained in a 2- or 3-compartment apparatus, with one of the compartments paired with drug over several conditioning trials and a placebo in the other compartment. Finally on a drug-free test day, the animal is given access to all compartments to see if they spend more time in the compartment that had been associated with the drug.

Textbook Reference: Factors That Influence the Development and Maintenance of Drug Abuse and Addiction 43. How does the conditioning model of addiction (as described by Wikler) explain relapse to drug use in the absence of actual withdrawal symptoms?

Answer: His argument is that if someone regularly uses a drug in a particular environment, the environmental cues (conditioned stimuli) become associated with the drug. Similarly, these cues can become associated with withdrawal. These environmental cues (even much later or if a person is drug-free) can induce a withdrawal syndrome in the presence of the same environment due to the conditioned cues, and this can initiate a withdrawal-like state which can then contribute to craving and relapse (classical conditioning).

Textbook Reference: Factors That Influence the Development and Maintenance of Drug Abuse and Addiction 44. Describe the three pathways linking personality to addiction.

Answer: The three different personality-related pathways to addiction are: • Behavioral disinhibition—deviant behaviors (like substance abuse) are linked to a cluster of traits (impulsivity, antisociality, unconventionality, and aggressiveness).

• Stress reduction—high anxiety and response to stress (and neuroticism); may be particularly vulnerable to stress; may use drugs to self-medicate.

• Reward sensitivity—personality characteristics including sensation seeking, reward seeking, extraversion, etc.; these traits may make these people seek out drugs that have positively rewarding effects.

Textbook Reference: Factors That Influence the Development and Maintenance of Drug Abuse and Addiction

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45. Describe some of the risk factors for developing drug addiction and some of the protective factors that may reduce risk.

Answer: There are a number of risk factors for developing a substance use disorder.

Some of these include starting with drugs at a younger age, less education, nonwhite ethnicity, unemployed, behavior problems as a child, substance-using friends, and stressful life events including childhood maltreatment, drug use in the home, etc.

Personality variables (already described above) can also be used to consider risk factors.

Protective factors can simply be an absence of many of the risk factors listed above— stable family, no pre-existing personality or mood disorder, etc. Other protective factors may help someone maintain their abstinence. These include avoiding environment or friends that have been associated previously with drugs (reducing cues), moving to a new place, finding new sources of support, and gaining financial stability.

Textbook Reference: Factors That Influence the Development and Maintenance of Drug Abuse and Addiction 46. What regions of the brain have been implicated in the preoccuptation/anticipation stage of drug use?

Answer: Brain imaging studies comparing addicted subjects with healthy controls have revealed both structural and functional abnormalities in the prefrontal cortex (PFC) in the addict group. The PFC has been implicated in executive function but also in regulation of emotion and motivational processes, and all of these may play a role in drug addiction. It has been argued that dysfunction in this region could play a role in intrusive thinking, craving, and lack of impulse control.

Textbook Reference: The Neurobiology of Drug Addiction 47. Describe two findings that counter the idea that dopamine is a ―pleasure neurotransmitter.‖ Answer: Certain drugs like THC and opiates provoke very little DA release in human striatum (from imaging studies). The dopaminergic system is essential for drug reward for some substances (e.g., cocaine or amphetamine) but not for others (e.g., heroin or alcohol).

Textbook Reference: The Neurobiology of Drug Addiction 48. Describe the neurochemical changes thought to underlie the transition from positive to negative reinforcement in addiction.

Answer: For some drugs, a physical withdrawal syndrome following chronic use can contribute to the continued use of drugs of addiction. Individuals begin taking these drugs for their positively rewarding effects; then, as compensatory changes occur in the brain and possibly elsewhere, they transition from taking the drug for the positive rewarding effects to taking the drug to avoid withdrawal (negative reinforcement).

Textbook Reference: The Neurobiology of Drug Addiction 49. Explain how the hedonic response to drug use changes during different stages of the addiction cycle. Be sure to include a description of the concept of allostasis.

Answer: This pertains to the opponent process theory to explain addiction. The premise is that initially if a drug makes a person feel good or high, there is an opposing affective

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response that is experienced after the initial stimulus ends. This subsequent opposing response is a dysphoric withdrawal reaction as the drug wears off. It has been proposed that allostasis plays a role in this cycle as well. Allostasis is a phenomenon in which the baseline hedonic state (i.e., mood) of the drug user gradually shifts with repeated drug use. Once the individual is dependent, the allostatic set point has shifted downward (0ʹ) and the baseline mood in the absence of the drug is negative (i.e., depressed mood, irritability, or anxiety). The positive hedonic response to the drug is nearly gone and the individual experiences very little reward, while the negative hedonic value is greatly increased (withdrawal), so there is significant pressure to take the drug for its negative reinforcing effects (i.e., to reduce withdrawal symptoms).

Textbook Reference: The Neurobiology of Drug Addiction 50. What is meant by the medicalization of drug addiction?

Answer: Medicalization of drug addiction refers to the idea that drug addiction is a disease and thus should be treated within the medical establishment.

Textbook Reference: The Neurobiology of Drug Addiction 51. What are some of the benefits and criticisms of the disease model of addiction?

Answer: Benefits—a medical model should remove the social stigma of addiction; allows for medical interventions and programs for treatment. Criticisms—claim that the data does not prove that addiction is a disease; some argue there is evidence against the disease concept; there is not a single diagnostic test to confirm if someone is addicted to a disease; some argue that addiction is a choice.

Textbook Reference: The Neurobiology of Drug Addiction

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Test Bank to accompany

Psychopharmacology, Third Edition Meyer • Quenzer

Chapter 10: Alcohol Multiple Choice 1. The first alcoholic beverage was a. a thick, hearty beer. b. mead. c. wine. d. gin.

Answer: b Textbook Reference: Psychopharmacology of Alcohol 2. During fermentation, yeast converts each molecule into two molecules of and two molecules of carbon dioxide. a. sugar; alcohol b. fat; alcohol c. alcohol; sugar d. sugar; fat Answer: a Textbook Reference: Psychopharmacology of Alcohol 3. Which of the following does not modify the concentration of alcohol in the blood? a. The presence of food in the stomach b. The dose of alcohol consumed c. Gender differences in metabolism d. A cold shower Answer: d Textbook Reference: Psychopharmacology of Alcohol 4. Eating while drinking alcohol alcohol absorption by emptying. a. increases; slowing down b. speeds up; increasing c. slows down; slowing down d. reduces; increasing Answer: c Textbook Reference: Psychopharmacology of Alcohol

gastric

5. The first step in the metabolism of alcohol is its conversion to a. formaldehyde.

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b. acetaldehyde. c. acetic acid. d. aldehyde dehydrogenase.

Answer: b Textbook Reference: Psychopharmacology of Alcohol 6. Which of the following best represents the enzymatic steps involved in alcohol metabolism? a. Alcohol → alcohol dehydrogenase → acetaldehyde → acetaldehyde dehydrogenase → acetic acid b. Alcohol → alcohol dehydrogenase → acetic acid → acetaldehyde dehydrogenase → acetaldehyde c. Alcohol → acetaldehyde dehydrogenase → acetaldehyde → alcohol dehydrogenase → acetic acid d. Alcohol → acetaldehyde dehydrogenase → acetic acid → alcohol dehydrogenase → acetaldehyde Answer: a Textbook Reference: Psychopharmacology of Alcohol 7. Alcohol is metabolized in the liver by two systems of enzymes, a. aldehyde dehydrogenase; cytochrome P450 b. alcohol dehydrogenase; acetaldehyde c. alcohol dehydrogenase; cytochrome P450 d. alcohol dehydrogenase; aldehyde dehydrogenase Answer: c Textbook Reference: Psychopharmacology of Alcohol

and

.

8. A decrease in activity can lead to toxicity, including flushing, nausea, and vomiting. a. alcohol dehydrogenase b. acetaldehyde dehydrogenase c. acetaldehyde d. formaldehyde Answer: b Textbook Reference: Psychopharmacology of Alcohol 9. tolerance to alcohol results from a(n) a. Metabolic; reduction b. Pharmacodynamic; reduction c. Metabolic; induction d. Acute; induction Answer: c Textbook Reference: Psychopharmacology of Alcohol

of liver enzymes.

10. In tolerance, the effects of alcohol falling compared to when they are rising.

when blood alcohol levels are

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a. acute; decrease b. acute; increase c. pharmacodynamic; increase d. acute; remain the same Answer: a Textbook Reference: Psychopharmacology of Alcohol 11. Tolerance to alcohol includes a. metabolic but not pharmacodynamic tolerance. b. pharmacodynamic but not behavioral tolerance. c. metabolic and pharmacodynamic tolerance. d. neither metabolic nor pharmacodynamic tolerance.

Answer: c Textbook Reference: Psychopharmacology of Alcohol 12. Which of the following is not a potential explanation for a hangover? a. Toxic effects of congeners in the alcohol b. Residual acetaldehyde in the body c. Excessive fluid loss during the drinking bout d. Residual acetic acid in the body Answer: d Textbook Reference: Psychopharmacology of Alcohol 13. An intense withdrawal syndrome after long-term heavy drinking that includes irritability, convulsions, and hallucinations would be considered a. delirium tremens. b. a hangover. c. psychosis. d. physical dependence.

Answer: a Textbook Reference: Psychopharmacology of Alcohol 14. During an individual may behave quite normally but will have total amnesia for the events that occurred. a. delirium tremens b. a blackout c. a hangover d. Wernicke−Korsakoff syndrome Answer: b Textbook Reference: Psychopharmacology of Alcohol 15. Alcohol is involved in about reduces . a. one-third; reaction time b. half; memory skills c. half; reaction time

of all highway deaths, in part because it

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d. two-thirds; memory Answer: a Textbook Reference: Psychopharmacology of Alcohol 16. A blood alcohol level of % is lethal in half of the population, but because unconsciousness occurs at a BAC of around %, drinking is often stopped before the lethal level is reached. a. 0.35; 0.15 b. 0.45; 0.1 c. 0.45; 0.35 d. 0.60; 0.1 Answer: c Textbook Reference: Psychopharmacology of Alcohol 17. Fatalities from acute alcohol ingestion occur because a. of cardiac arrhythmias leading to heart failure. b. the respiratory centers in the brain stem shut down. c. the heart becomes too sedated and stops beating. d. that much alcohol causes brain death.

Answer: b Textbook Reference: Psychopharmacology of Alcohol 18. The memory disturbances seen in Wernicke-Korsakoff syndrome include a. a loss of memory for events in the distant past. b. total amnesia. c. a loss of short-term, immediate memory with retention of distant memories. d. little actual memory impairment.

Answer: c Textbook Reference: Psychopharmacology of Alcohol 19. While widespread brain damage can be seen in alcoholics, thiamine deficiency causes specific damage to the a. cerebellum. b. frontal cortex. c. hippocampus. d. thalamus Answer: d Textbook Reference: Psychopharmacology of Alcohol 20. Limited alcohol consumption (less than three drinks per day) may improve cognitive function by a. reducing the risk of stroke. b. increasing blood flow, and thus oxygen, to the brain. c. decreasing ―bad ‖ cholesterol. d. increasing ―good‖ cholesterol.

Answer: b

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Textbook Reference: Psychopharmacology of Alcohol 21. Fatty liver occurs because of a buildup of , while cirrhosis is the result of the formation of . a. acetaldehyde; scar tissue b. scar tissue; triglycerides c. triglycerides; scar tissue d. acetaldehyde; triglycerides Answer: c Textbook Reference: Psychopharmacology of Alcohol 22. Which of the following is not a sign of fetal alcohol syndrome? a. Abnormally high birth weight b. Neurological problems c. Mental retardation d. Craniofacial malformations Answer: a Textbook Reference: Psychopharmacology of Alcohol 23. Understanding the neurochemical effect of alcohol is difficult because a. animals will not spontaneously drink enough alcohol to become intoxicated. b. alcohol can affect multiple organ systems. c. alcohol does not affect specific receptor proteins. d. alcohol can alter the fluidity of the lipid bilayer of cell membranes.

Answer: d Textbook Reference: Neurochemical Effects of Alcohol 24. can be used to assess genetic differences between animals that differ in some alcohol-related behavior, while are used to determine the role of a particular protein in alcohol’s effects. a. Selectively bred lines; knockout animals b. Knockout animals; genetic screens c. Selectively bred lines; genetic screens d. Genetic screens; selectively bred lines Answer: a Textbook Reference: Neurochemical Effects of Alcohol 25. The specific actions of alcohol on neuronal membranes include all of the following except a. direct interactions with channel proteins. b. modification of gating mechanisms inside a channel. c. actions at neurotransmitter binding sites. d. alteration of lipid composition.

Answer: d Textbook Reference: Neurochemical Effects of Alcohol

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26. Acute alcohol the effectiveness of glutamate at NMDA receptors and glutamate release. a. reduces; increases b. increases; increases c. increases; reduces d. reduces; reduces Answer: d Textbook Reference: Neurochemical Effects of Alcohol 27. After withdrawal from chronic alcohol use, an increase in an increase in behavioral signs of . a. glutamate release; intoxication b. glutamate release; withdrawal hyperexcitability c. receptor inhibition; intoxication d. receptor inhibition; withdrawal hyperexcitability Answer: b Textbook Reference: Neurochemical Effects of Alcohol

is correlated with

28. Alcohol and benzodiazepines most likely show cross-tolerance and cross-dependence because they both the effects of at receptors. a. decrease; glutamate; NMDA b. enhance; glutamate; NMDA c. decrease; GABA; GABA A d. enhance; GABA; GABA A Answer: d Textbook Reference: Neurochemical Effects of Alcohol and chronic alcohol _ GABA A-mediated chloride flux.

29. Acute alcohol a. enhances; inhibits b. inhibits; inhibits c. enhances; enhances d. inhibits; enhances Answer: a Textbook Reference: Neurochemical Effects of Alcohol 30. Alcohol increases synaptic levels of dopamine in the nucleus accumbens by a. blocking the reuptake of dopamine by transporters. b. increasing the firing rate of cells in the VTA. c. inhibiting the metabolism of dopamine in the synaptic cleft. d. decreasing action of autoreceptors which normally decrease release.

Answer: b Textbook Reference: Neurochemical Effects of Alcohol 31. Which of the following is not seen during alcohol withdrawal? a. Decrease in dopamine levels in the nucleus accumbens b. Increase in the amount of current needed for intracranial brain stimulation

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c. Increase in glutamate release d. Increase in chloride flux through GABA A receptors Answer: d Textbook Reference: Neurochemical Effects of Alcohol 32. are two neurotransmitters that most likely are involved in the reinforcing effects of alcohol. a. GABA and serotonin b. Dopamine and the opioids c. Norepinephrine and serotonin d. Glutamate and GABA Answer: b Textbook Reference: Neurochemical Effects of Alcohol 33. Changes in which two neurotransmitter systems are most likely involved in the hyperexcitability seen during withdrawal from chronic alcohol? a. GABA and glutamate b. GABA and dopamine c. Dopamine and glutamate d. The opioids and dopamine Answer: a Textbook Reference: Neurochemical Effects of Alcohol 34. Which statement about the role of the endogenous opioid system in alcohol’s reinforcing effects is false? a. Mice that lack the μ-opioid receptor do not self-administer alcohol. b. Opioid receptor antagonists reduce alcohol self-administration in animals. c. Clinical trials show that opioid receptor antagonists decrease relapse to drinking in humans. d. Chronic alcohol use increases gene expression of endorphin and enkephalin.

Answer: d Textbook Reference: Neurochemical Effects of Alcohol 35. In general, the cellular effects of chronic alcohol on various neurotransmitter systems are the effects of acute alcohol administration. a. the same as b. opposite to c. double d. many times greater than Answer: b Textbook Reference: Neurochemical Effects of Alcohol 36. Binge drinking is defined as a. any rapid consumption of alcohol that causes intoxication. b. drinking until passing out. c. five or more drinks in a row for males and four in a row for females.

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d. drinking to remain intoxicated for at least two days.

Answer: c Textbook Reference: Alcohol Use Disorder (AUD) 37. According to Cloninger’s alcoholic subtypes, type II alcoholics are characterized by a. a high extent of genetic influence, age of onset before 25, and thrill-seeking behavior. b. a high extent of genetic influence, age of onset after 25, and guilt and fear about alcohol. c. age of onset after 25, inability to stop alcohol use, and low incidence of noveltyseeking personality. d. being either male or female, use of alcohol to escape, and a moderate extent of genetic influence.

Answer: a Textbook Reference: Alcohol Use Disorder (AUD) 38. In the method of genetic study, genes of affected and unaffected individuals who are not related are compared to search for alleles that may be common among affected individuals. a. selective breeding b. linkage study c. case-control d. family history Answer: c Textbook Reference: Alcohol Use Disorder (AUD) 39. In Schuckit’s study, a greater risk of developing alcoholism was seen in young men who experienced _ subjective ―high‖ and had a sway score after consuming alcohol. a. a greater; lower b. a greater; higher c. less of a; higher d. less of a; lower Answer: d Textbook Reference: Alcohol Use Disorder (AUD) 40. Disulfiram makes consumption of alcohol unpleasant because it a. blocks the conversion of alcohol to acetaldehyde. b. blocks the conversion of acetaldehyde to acetic acid. c. blocks μ-opioid receptors. d. acts as a partial agonist at NMDA receptors.

Answer: b Textbook Reference: Alcohol Use Disorder (AUD) 41. In animal models, blockade of reduces stress-induced relapse and withdrawal-induced alcohol consumption, but this approach hasn’t worked in humans because .

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a. opioid receptors; people just won’t take the medication b. NK1R; humans don’t possess this receptor type c. CRF1 receptors; these antagonists don’t cross the blood–brain barrier d. glutamate receptors; stress is not a major factor in human alcohol consumption Answer: c Textbook Reference: Alcohol Use Disorder (AUD)

Short Answer/Essay 42. Compare and contrast pharmacodynamic, metabolic, and behavioral tolerance.

Answer: Pharmacodynamic tolerance occurs when cells become less responsive to alcohol. This has also been called cellular tolerance. Metabolic tolerance occurs when the body increases its ability to metabolize alcohol, thus breaking it down quicker and producing less alcohol in the blood. Behavioral tolerance refers to the adaptations in behavior that can be made to improve performance while exposed to alcohol.

Textbook Reference: Psychopharmacology of Alcohol 43. How can classical conditioning contribute to behavioral tolerance?

Answer: Given cues, such as administering alcohol in the same environment each time, may trigger the body to make responses to counter the effects of alcohol. This could promote behavioral tolerance.

Textbook Reference: Psychopharmacology of Alcohol 44. Describe the ways males and females differ with regard to the effects of alcohol.

Answer: As a group, females have less metabolic activity towards alcohol compared to males, in large part due to less activity of alcohol dehydrogenase in the stomach. Aspirin will inhibit metabolism more in females, and a higher fat/muscle ratio in females will mean a greater blood alcohol level, since fat doesn’t contain as much water (to mix with the alcohol) as muscle. A smaller body size in females will also contribute to alcohol being at a higher blood level in females, again due to less body water to dilute the alcohol.

Textbook Reference: Psychopharmacology of Alcohol 45. Describe the evidence that the expectation of alcohol alone can influence behavior.

Answer: One example would be to create four groups of people. Two of the groups are told they will receive alcohol; two are told they will not receive alcohol. For the test, one group that was told they would receive alcohol does receive alcohol; for the groups told they would not receive alcohol, one group actually does receive alcohol. The drugs administered to all groups are disguised so that the subjects cannot tell by taste, smell, etc. what drugs they received. Researchers then evaluate behavioral responses and distinguish if expectation of receiving alcohol plays a role in determining behavioral response.

Textbook Reference: Psychopharmacology of Alcohol 46. Describe the effects of alcohol on sleep.

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Answer: With increasing dosage, sedation increases and the drive for sleep increases.

Rapid eye movement (REM) sleep is inhibited, and can rebound during alcohol withdrawal.

Textbook Reference: Psychopharmacology of Alcohol 47. Explain how limited consumption of alcohol can actually improve health.

Answer: Moderate drinking may increase blood flow to the brain and decrease risk of dementia associated with poor blood flow in the brain, and may reduce the risk of heart disease, blood clots, and stroke.

Textbook Reference: Psychopharmacology of Alcohol 48. Describe three ways animal models can make important contributions to alcohol research.

Answer: Genetic alterations can be produced to study the role of specific genes in alcohol consumption. Environmental conditions, including diet, can be controlled, so that alcohol usage can be the only variable. Animal models of alcohol addiction can be used to screen for possible pharmacological tools to treat human alcohol addiction.

Textbook Reference: Neurochemical Effects of Alcohol 49. Describe the evidence that intoxicating concentrations of alcohol alter GABAA receptor function.

Answer: Alcohol can potentiate the increase in chloride permeability that occurs when GABA binds to the GABA A receptor; some alcohol effects can be blocked by GABA A antagonists, such as bicuculline and picrotoxin; mice bred for greater sensitivity to alcohol also have a more sensitive response to alcohol’s effects on the GABA A system.

Textbook Reference: Neurochemical Effects of Alcohol 50. How can the effects of chronic alcohol on GABA and glutamate systems be related to tolerance and signs of withdrawal?

Answer: If alcohol’s potentiating effect on GABA A receptors leads to a down-regulation of these receptors, tolerance could occur, and the down regulation could lead to less neuronal inhibition during alcohol withdrawal, which could contribute to seizure activity.

Conversely, if glutamate is inhibited by alcohol, this system may up-regulate, which could also contribute to tolerance, and the increased glutamate state may also contribute to hyper-excitability of the nervous system during alcohol withdrawal, and work with the changes in GABA to produce seizures.

Textbook Reference: Neurochemical Effects of Alcohol 51. Describe some of the contributing factors to alcoholism according to the three-factor vulnerability model.

Answer: The three factors are psychological, neurobiological, and sociocultural. For psychological factors, stress can contribute to excessive alcohol usage in an attempt to relieve the feeling of stress; but ironically, excessive alcoholic use can itself become a stress. Anxiety disorders are often found to coexist with alcohol addiction.

Neurobiological factors include genetic influences. For instance, the rate of alcohol addiction is higher (about double) in monozygotic twins compared to dizygotic twins.

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Sociocultural factors can be seen with regard to group attitudes towards drinking. For instance, the rate of alcohol addiction is relatively low in groups (such as Mormons and Muslims) who have rules against alcohol consumption.

Textbook Reference: Alcohol Use Disorder (AUD) 52. How are naltrexone and acamprosate thought to decrease relapse rates in alcoholics?

Answer: Naltrexone is an opiate receptor antagonist, and, as such, can block circuits in the brain that make use of opiate peptide neurotransmitters. It is possible that circuits activated by excessive alcohol usage may produce a craving for alcohol, and these circuits could be inhibited by naltrexone. Acamprosate has several pharmacological actions, including reducing glutamate activity in the brain, and it may also increase GABA activity.

Textbook Reference: Alcohol Use Disorder (AUD)

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Test Bank to accompany

Psychopharmacology, Third Edition Meyer • Quenzer

Chapter 11: The Opioids Multiple Choice 1. All of the following are effects of the class of drugs called narcotic analgesics except a. relaxation. b. diarrhea. c. pain reduction. d. euphoria.

Answer: b Textbook Reference: Narcotic Analgesics 2. Which statement about opium is false? a. It has a long history of recreational use but has only recently been used medicinally. b. It was once a popular remedy for women, in the form of laudanum. c. It replaced alcohol as the most popular recreational drug in some cultures. d. It was given to infants and children.

Answer: a Textbook Reference: Narcotic Analgesics 3. What was the view toward opiates in the late 1800s and early 1900s? a. Individual states had begun to exert tight controls over access to opiates. b. The federal government passed the Harrison Narcotics Act in 1886, essentially controlling all opiate transactions. c. There was very little concern about safety, addiction, or health issues related to opiate use. d. Physicians had to report their prescriptions for opiates to the government, but there was no general concern.

Answer: c Textbook Reference: Narcotic Analgesics 4. All of the following are naturally occurring opiates except a. thebaine. b. codeine. c. morphine. d. heroin.

Answer: d Textbook Reference: Narcotic Analgesics 5. Heroin is

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a. converted to morphine in the brain. b. less lipid-soluble than morphine. c. a partial agonist at the opiate receptor. d. more potent than morphine if taken by mouth.

Answer: a Textbook Reference: Narcotic Analgesics 6. Which statement about pure opiate antagonists is false? a. They include drugs like naloxone and nalorphine. b. They are important in understanding the action of opiate analgesics. c. They can reverse the effects of an opiate overdose in approximately two hours. d. They have structures similar to opiates but produce no activity at the receptor.

Answer: c Textbook Reference: Narcotic Analgesics 7. Which drug would be considered a partial agonist? a. Codeine b. Pentazocine c. Methadone d. Hydromorphone Answer: b Textbook Reference: Narcotic Analgesics 8. All of the following are synthetic opiate drugs except a. fentanyl. b. propoxyphene. c. LAAM. d. codeine.

Answer: d Textbook Reference: Narcotic Analgesics 9. Opiate drugs used medically are usually administered a. orally. b. via inhalation/smoking. c. intranasally (snorting). d. via subcutaneous injection.

Answer: a Textbook Reference: Narcotic Analgesics 10. At low doses, opiates exert all of the following effects except a. pain relief. b. pupil dilation. c. drowsiness. d. depressed respiration.

Answer: b Textbook Reference: Narcotic Analgesics

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11. One common effect of increasing opiate dose is a. euphoria. b. elevated respiration rate. c. increased sex drive. d. increased awareness of one’s surroundings.

Answer: a Textbook Reference: Narcotic Analgesics 12. Opiates are dangerous at high doses due mostly to a. their effects on cardiac muscle. b. the increased likelihood of a stroke. c. the suppression of the brain stem’s respiratory center. d. an overstimulation of the sympathetic nervous system.

Answer: c Textbook Reference: Narcotic Analgesics 13. The nociceptin/orphanin FQ receptor (NOP-R) a. is genetically related to the classical opioid receptors, μ, δ, and κ. b. has a high binding affinity for the endogenous opioids. c. is found only in limbic areas and the spinal cord. d. produces euphoria when activated.

Answer: a Textbook Reference: Narcotic Analgesics 14. Peripherally acting opiate drugs have a specific therapeutic use that is also an unfortunate side effect of some opiate medications/drugs. Which of the following is this side effect? a. Reduction in saliva b. Slowing of gastrointestinal function/motility c. Decrease in body temperature d. Decrease in appetite Answer: b Textbook Reference: Narcotic Analgesics 15. Which of the following is not one of the ways Pert and Snyder confirmed that they had in fact located and labeled opiate receptors? a. They showed that the binding of radioactive naloxone increased in a linear fashion until all receptors were fully occupied, then it leveled off. b. They showed that the binding sites have a high affinity for the opiates tested. c. They demonstrated that the binding and the physiological effects were completely irreversible. d. They showed that the drug concentrations in the binding assay were similar to those needed to elicit a biological response.

Answer: c Textbook Reference: Opioid Receptors and Endogenous Neuropeptides

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16. Which preparation was used to initially study the effects of pharmacological agents on the opiate receptor? a. Guinea pig ileum b. Spinal cord preparation c. Cortical slice d. Hippocampal slice Answer: a Textbook Reference: Opioid Receptors and Endogenous Neuropeptides 17. The μ-receptor a. has been linked to hallucinations and dysphoria. b. overlaps with the κ-receptor in its distribution in the nervous system. c. is found in the hypothalamus and pituitary. d. plays a role in analgesia and the rewarding effects of morphine.

Answer: d Textbook Reference: Opioid Receptors and Endogenous Neuropeptides 18. What do we know about the structure of the opiate receptors from receptor cloning studies? a. Each receptor has between 650 and 700 amino acids. b. The receptors appear to be metabotropic. c. Each receptor has twelve transmembrane proteins. d. Each receptor will bind to the same ligands in the same way.

Answer: b Textbook Reference: Opioid Receptors and Endogenous Neuropeptides 19. Which of the following is not a larger propeptide that is broken down into smaller active opioids? a. Prodynorphin b. Proenkephalin c. Proendomorphin d. Pro-opiomelanocortin Answer: c Textbook Reference: Opioid Receptors and Endogenous Neuropeptides 20. The opioid propeptides a. are made in the terminal button and cleaved by enzymes into the opiate peptides. b. are processed by proteases into both opiate and non-opioid peptides. c. are referred to as the ―enkephalins.‖ d. include the endorphins and the endomorphins.

Answer: b Textbook Reference: Opioid Receptors and Endogenous Neuropeptides 21. Which statement about POMC is false? a. POMC is the propeptide for the dynorphins.

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b. Foot shock and swim stress increase POMC. c. POMC is found in high concentration in the pituitary gland. d. POMC is implicated in stress-induced analgesia.

Answer: a Textbook Reference: Opioid Receptors and Endogenous Neuropeptides 22. The peptide nociceptin/orphanin FQ (N/OFQ) a. enhances opioid-mediated analgesia in supraspinal regions. b. enhances motor performance. c. is an analgesic at the spinal level. d. suppresses feeding behavior.

Answer: c Textbook Reference: Opioid Receptors and Endogenous Neuropeptides 23. is the natural ligand for the -receptor. a. Dynorphin b. Nociceptin/orphanin FQ c. Endorphin d. Enkephalin Answer: d Textbook Reference: Opioid Receptors and Endogenous Neuropeptides 24. Which statement about the effects of opiates on synaptic transmission is false? a. They act on receptors that are coupled to G proteins that open potassium channels, close calcium channels, and inhibit adenylyl cyclase. b. They affect presynaptic autoreceptors and reduce the amount of transmitter released. c. They cause postsynaptic depolarization by opening potassium channels. d. They cause less transmitter to be released via axoaxonic inhibition.

Answer: c Textbook Reference: Opioid Receptors and Endogenous Neuropeptides 25. Postsynaptic inhibition by endorphins is caused by of a. opening; chloride b. opening; potassium c. closing; calcium d. closing; potassium Answer: b Textbook Reference: Opioid Receptors and Endogenous Neuropeptides

channels.

26. Nociceptors detect a. intense pressure. b. extreme temperature. c. chemical irritants. d. All of the above Answer: d Textbook Reference: Opioids and Pain

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27. The effects of analgesics on pain are difficult to study because a. it is impossible to obtain subjective reports of pain. b. the results depend on the specific technique being used to produce pain. c. ethical guidelines prohibit the application of painful stimuli to animals. d. humans refuse to participate in the research.

Answer: b Textbook Reference: Opioids and Pain 28. ―First‖ or early pain a. typically triggers withdrawal and escape responses. b. provides information about the unpleasantness of the painful sensation. c. is transmitted by neural pathways to the limbic system. d. is often accompanied by autonomic responses, such as nausea.

Answer: a Textbook Reference: Opioids and Pain 29. When you stub your toe on a hard object, the lingering ache you feel after the initial sharp pain has worn off is caused by a. pain messages traveling in A fibers. b. input reaching the somatosensory cortex and then being processed in adjacent areas. c. information being carried in slowly conducting unmyelinated fibers. d. rapid adaptation occurring at spinal cord levels.

Answer: c Textbook Reference: Opioids and Pain 30. Both ―early‖ and ―late‖ pain activate the a. primary somatosensory cortex. b. anterior cingulate cortex. c. amygdala. d. secondary somatosensory cortex.

Answer: d Textbook Reference: Opioids and Pain 31. Pain transmission in the spinal cord can be blocked by a. the action of inhibitory spinal interneurons that release endorphins. b. deactivating descending pathways from the forebrain that enhance the pain pathway. c. turning off ascending pathways that activate endorphin interneurons. d. All of the above Answer: a Textbook Reference: Opioids and Pain 32. The most important descending pathways for modulation of spinal cord transmission of pain originate in the a. thalamus. b. midbrain PAG.

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c. limbic system. d. anterior cingulate cortex.

Answer: b Textbook Reference: Opioids and Pain 33. Electrical stimulation of the PAG a. produces changes in sensations of touch and pressure. b. produces a type of analgesia that is not blocked by naloxone. c. activates dopamine cells in the medulla, which in turn inhibit spinal cord pain transmission. d. most likely releases endogenous opiates that act on μ- and κ-receptors.

Answer: d Textbook Reference: Opioids and Pain 34. Which statement about pain perception and opiate action at supraspinal levels is false? a. This aspect of pain is often referred to as the affective component of pain. b. Pain reduction at supraspinal levels is primarily mediated by δ-receptors. c. Endocrine and autonomic responses to pain are controlled from these levels. d. PET scans show a negative correlation between μ-receptor activation in several limbic structures and emotional pain scores.

Answer: b Textbook Reference: Opioids and Pain 35. Which statement about other forms of pain control is true? a. Acupuncture-induced analgesia is blocked by µ-receptor antagonists. b. Although inhibiting the two peptidases that degrade enkephalin produces significant analgesia, addiction potential is a concern. c. An initial gene therapy trial used a virus engineered to contain the gene coding for human proenkephalin. d. Although NOP-R agonists reduce pain, their use is limited by side effects such as constipation and respiratory depression.

Answer: c Textbook Reference: Opioids and Pain 36. Some researchers believe that opiates exert their effects on reinforcement by affecting cell bodies in the that release . a. nucleus accumbens; GABA b. nucleus accumbens; dopamine c. VTA; GABA d. VTA; dopamine Answer: d Textbook Reference: Opioid Reinforcement, Tolerance, and Dependence 37. A model of the neurobiology of opiate reinforcement suggests that opiates produce their effects by inhibiting neurons.

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a. dopamine b. GABA c. dynorphin d. β-endorphin Answer: b Textbook Reference: Opioid Reinforcement, Tolerance, and Dependence 38. Tolerance to opiate effects a. is primarily due to increased rate of metabolism. b. develops quite gradually over time. c. is not specific to a given receptor type. d. occurs rapidly for analgesic effects and slowly for constipating effects.

Answer: d Textbook Reference: Opioid Reinforcement, Tolerance, and Dependence 39. The opiate withdrawal or abstinence syndrome a. can be explained as a form of rebound CNS hyperactivity. b. is considered to be a life-threatening condition. c. involves intense inhibitory opiate action at all receptors. d. lasts for about 48 hours; the user is then considered detoxified.

Answer: a Textbook Reference: Opioid Reinforcement, Tolerance, and Dependence 40. Which brain area has not been implicated in the opiate withdrawal syndrome? a. PAG b. Amygdala c. Frontal cortex d. Locus coeruleus Answer: c Textbook Reference: Opioid Reinforcement, Tolerance, and Dependence 41. Himmelsbach’s classic model of opiate dependence as a disruption of homeostasis was confirmed physiologically by studying a. changes in cAMP synthesis. b. intracerebral injections of opiate antagonists. c. place aversion for novel environments. d. mechanisms underlying classical conditioning tolerance.

Answer: a Textbook Reference: Opioid Reinforcement, Tolerance, and Dependence 42. Which factor does not increase the risk of opioid misuse? a. Psychosocial stress b. Older age c. Genetic variant d. Chronic pain condition Answer: b

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Textbook Reference: Opioid Reinforcement, Tolerance, and Dependence 43. CDC federal guidelines for pain control a. are intended to reduce opioid deaths and opioid abuse. b. recommend the use of aspirin or physical therapy rather than opiates. c. make some physicians uneasy when they cannot relieve their patients’ suffering. d. All of the above Answer: d Textbook Reference: Opioid Reinforcement, Tolerance, and Dependence 44. Treatment programs for opiate addicts a. have shown that unassisted detoxification, or going ―cold turkey,‖ is a very effective method. b. sometimes employ the opiate antagonist buprenorphine. c. typically use methadone maintenance strategies. d. have recently incorporated the use of clonidine for blocking the opiate receptors in highly motivated addicts.

Answer: c Textbook Reference: Treatment Programs for Opioid Use Disorder 45. Which of the following is not a reason why methadone is an effective treatment for opiate drug abuse? a. It is a long-lasting drug, producing stable blood levels throughout the day. b. It is cross-tolerant with abused opiates, so it can reduce the effects of morphine and heroin with repeated use. c. It produces no euphoria or craving when administered orally in clinics. d. It has no reinforcing effect, even if administered intravenously.

Answer: d Textbook Reference: Treatment Programs for Opioid Use Disorder 46. Which of the following is not an advantage of buprenorphine maintenance compared to methadone maintenance? a. Buprenorphine’s shorter duration of action reduces the chance of overdose. b. Buprenorphine can be administered with subcutaneous implants. c. Buprenorphine does not require daily clinic visits. d. Neonatal abstinence syndrome is milder in buprenorphine withdrawal.

Answer: a Textbook Reference: Treatment Programs for Opioid Use Disorder

Short Answer/Essay 47. Distinguish between naturally occurring opiates, synthetic opiates, semisynthetic opiates, and endogenous opioids. Provide examples of each.

Answer: Naturally occurring opiates are those derived from the opium poppy, such as codeine and morphine. If chemical modification of the natural opiate is required, the

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drugs, such as heroin, are considered semisynthetic. Totally synthetic opioids like meperidine have very distinct structures. Endogenous opioids or endorphins are neuropeptides synthesized from large propeptides in the CNS and other tissues.

Textbook Reference: Narcotic Analgesics 48. Identify the four different types of opiate receptors and the endogenous ligands that show a relative preference for the receptor. Identify three potential roles for each.

Answer: Endomorphins and endorphins show a relative preference for the µ-receptor.

They have a role in morphine-induced analgesia, respiratory depression, and positive reinforcement. Enkephalin and endorphins bind to the -receptor and play a part in modulating motor integration, reinforcement, and cognitive function. Dynorphins bind to κ-receptors and modulate gut motility, dysphoria, and neuroendocrine function.

Nociceptin/orphanin FQ is the endogenous ligand for the NOP-R and has a role in analgesia, learning, and neuroendocrine regulation.

Textbook Reference: Opioid Receptors and Endogenous Neuropeptides 49. How were the endogenous ligands for the opiate receptors discovered? Name the four propeptides and give their approximate location. What is unique about the endomorphins?

Answer: The opioids were discovered in brain extracts and were shown to bind to opioid receptors and mimic opioid activity electrophysiologically and in bioassays. The propeptides are prodynorphin, POMC, proenkephalin, and pronociceptin/orphanin FQ. They are found in the CNS and peripheral ANS where they are concentrated in areas related to pain modulation and mood. POMC is also concentrated in the pituitary gland.

The propeptide for endomorphins has not been found.

Textbook Reference: Opioid Receptors and Endogenous Neuropeptides 50. Describe the three basic ways that endorphins can exert inhibitory effects on synaptic transmission.

Answer: Opioids have inhibitory effects by binding to receptors that activate a G protein that opens potassium channels to hyperpolarize the postsynaptic cells. They also act on receptors on nerve terminals that activate G proteins that close calcium channels, reducing neurotransmitter release. Opioids also act on presynaptic autoreceptors that activate G proteins that reduce the release of a co-localized neurotransmitter.

Textbook Reference: Opioid Receptors and Endogenous Neuropeptides 51. Distinguish between ―first‖ and ―second‖ pain in terms of the nature of pain information being transmitted, the speed of the transmission, and the neural pathways activated.

Answer: First pain signals the immediate sensory component of a noxious stimulus and informs its precise location. It causes rapid withdrawal from the damaging stimulus. First pain is carried rapidly on myelinated A fibers and after going to the thalamus via the lateral spinothalamic tract, it relays to primary and secondary somatosensory cortex.

Second pain is slower and more persistent and represents the unpleasantness of the sensation. The sensory information is carried on slower unmyelinated C fibers and also

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goes to the thalamus but gives off collaterals to limbic areas and anterior cingulate cortex before going to secondary somatosensory cortex.

Textbook Reference: Opioids and Pain 52. How has MEG technology helped to distinguish between fast and slow pain systems?

Answer: MEG technology has been able to visualize in real time the first and second pain components. By exposing subjects to brief painful stimuli and recording their pain ratings while monitoring the change in cortical magnetic fields on the skull, they could see that first pain was associated with activation of the primary somatosensory cortex and second pain was associated with the anterior cingulate cortex.

Textbook Reference: Opioids and Pain 53. Describe the basic ways that opioids can inhibit or reduce the transmission of pain at spinal levels. Where do some of these inhibitory pathways originate?

Answer: Pain signals on projection neurons going to higher brain centers can be inhibited in the spinal cord by small spinal interneurons that release endorphins. Endorphins also regulate two modulatory pathways originating in PAG that descend to the raphe nucleus and locus coeruleus. From there, neurons descend to spinal cord to inhibit the projection neuron or an excitatory interneuron, or by exciting the inhibitory opioid neuron.

Textbook Reference: Opioids and Pain 54. What type of pain is being modulated at supraspinal levels? Identify the brain areas that are involved in opiate modulation of pain at the supraspinal level.

Answer: Supraspinal brain regions may be responsible for the emotional component of pain including autonomic and neuroendocrine responses. High concentrations of opioids and opioid receptors are found in higher sensory areas, limbic structures, as well as hypothalamus and medial thalamus.

Textbook Reference: Opioids and Pain 55. Provide evidence to show that the analgesic effect of electroacupuncture is dependent on opioids. Which opioid peptide is responsible?

Answer: Electroacupuncture-induced analgesia can be prevented by pretreatment with naloxone. A κ-receptor antagonist prevents analgesia induced by 100-Hz electroacupuncture but not that induced by 2 Hz. Also, 100-Hz acupuncture shows crosstolerance to κ-agonists but not -agonists, and increases levels of dynorphin. In contrast, a -antagonist blocked analgesia following 2-Hz but not 100-Hz acupuncture. Also, 2-Hz stimulation showed cross-tolerance with - but not κ-agonists, and it raised levels of proenkephalin.

Textbook Reference: Opioids and Pain 56. What is the rationale for the development of dual µ-receptor/NOP-R agonists? What research findings suggest these agents have clinical potential as analgesics?

Answer: NOP-R agonists have analgesic action so less µ-receptor stimulation will be needed and side effects will be less. Research showed dose-dependent analgesia with the dual agonists that was very long-lasting. Not only was there no physical dependence as shown by lack of withdrawal, but self-administration tests showed little reinforcement

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and hence low abuse potential. Further, its therapeutic index is better than morphine because it produces less respiratory depression and cardiovascular effects.

Textbook Reference: Opioids and Pain 57. What are the factors that may help clinicians identify individuals who are vulnerable to potential opiate abuse and overdose and minimize that risk?

Answer: One study showed that emergency room patients who were treated by ―highintensity‖ opioid-prescribing physicians were more likely to develop long-term opioid use than those treated by ―low-intensity‖ prescribers. Other research showed that a gene polymorphism that reduces mRNA expression leading to reduced µ-receptor levels, altered β-endorphin binding affinity, and altered HPA axis response was associated with vulnerability to heroin addiction and overdose severity. Another factor is the treatment of chronic pain conditions. Physicians are encouraged to treat pain with aspirin and ibuprofen rather than opiates and to utilize alternative approaches for pain control, such as physical therapy, acupuncture, cognitive behavior therapy, and others.

Textbook Reference: Opioid Reinforcement, Tolerance, and Dependence 58. Cite evidence showing that dopamine plays a key role in the reinforcing value of opiates. Identify two dopamine brain areas that are particularly important in this role.

Researchers have recently proposed that dopamine is not required for this rewarding effect. Explain this statement.

Answer: Animals will self-administer opioids when the microinjection is into VTA cell bodies of the DA reinforcement pathway, and the same microinjection produces conditioned place preference and reduces the threshold for intracranial electrical self simulation. Systemic or intra-VTA opioids increase DA cell firing and release of DA in NAcc. DA receptor antagonists block opioid reinforcement; however, other mechanisms must be involved because destroying the DA neurons only partially reduces selfadministration.

Textbook Reference: Opioid Reinforcement, Tolerance, and Dependence 59. Distinguish between tolerance, cross-tolerance, and sensitization. What physiological mechanism best explains opiate tolerance?

Answer: Tolerance refers to the diminishing effects of a drug with repeated use. Crosstolerance exists when tolerance develops to one drug and other chemically related drugs also show a reduced effectiveness even if the individual has never used those drugs previously. Sensitization refers to the increase in drug effects that occurs with repeated administration. Tolerance for opiates can be caused by a minor increase in rate of metabolism or by classical conditioning, but most is due to compensatory changes in nerve cells, such as a gradual compensatory increase in firing rate of locus coeruleus neurons as well as a rebound overshoot of cAMP synthesis.

Textbook Reference: Opioid Reinforcement, Tolerance, and Dependence 60. Describe the symptoms, time course, and seriousness of opiate withdrawal. What parts of the brain appear to be involved in the abstinence syndrome?

Answer: Opiate withdrawal symptoms are unpleasant but not life-threatening and include pain, dysphoria, restlessness, fearfulness, and flu-like symptoms. The severity and

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duration depends on the particular drug, drug dose, frequency and duration of use, and the health and personality of the addict. Intracerebral injection of an opioid antagonist into the locus coeruleus and PAG of a physically dependent rodent produces signs of withdrawal, implicating these brain areas. Injection into NAcc may be responsible for the aversive stimulus effects of withdrawal.

Textbook Reference: Opioid Reinforcement, Tolerance, and Dependence 61. Describe the basic components of Himmelsbach’s model of tolerance and withdrawal, and provide physiological evidence that supports his ideas.

Answer: The model suggests that acute morphine disrupts an organism’s homeostasis, but with repeated drug exposure, an adaptive mechanism gradually compensates and homeostasis returns (tolerance). When the drug is abruptly removed, the drug’s effects are ended but the adaptive mechanism remains so homeostasis is disrupted again (withdrawal). Researchers found acute hyperpolarizing effects of opioids in the locus coeruleus but gradual increased firing with repeated exposure (tolerance) and a rebound rise in firing rate to well above pretreatment levels with drug termination (withdrawal). A similar pattern was found earlier for the initial inhibition of cAMP synthesis, gradual return to toward normal with repeated exposure, and rebound elevation at withdrawal.

Textbook Reference: Opioid Reinforcement, Tolerance, and Dependence 62. Explain how environmental cues can (1) contribute to the development of tolerance and (2) act as secondary reinforcers to strengthen drug-taking behavior and cause relapse.

Answer: Classically conditioned environmental cues have a role in opiate tolerance.

When an animal regularly gets a drug in a particular environment, the environment acts as a cue associated with the drug’s effects. In response, the animal in that particular environment may show anticipatory, compensatory physiological responses which diminish the drug effects. Also, if drug-induced euphoria becomes closely associated with components of the drug-taking behavior, those environmental stimuli become cues and secondary reinforcers to trigger further drug taking and increased probability of relapse after abstinence.

Textbook Reference: Opioid Reinforcement, Tolerance, and Dependence 63. Distinguish between the following treatments for opiate abuse: detoxification, maintenance, use of antagonists, and counseling. Mention therapeutic drugs, when relevant.

Answer: Detoxification or the elimination of the drug from the body can be unassisted (―cold turkey‖) or assisted by administration of a long-acting opioid which is gradually tapered over a period of time. After detox, methadone or buprenorphine maintenance involves the long-term substitution of one opioid drug for another. By relieving craving, the addict can engage in more productive behaviors that don’t involve securing the abused drug. For highly motivated addicts, opioid antagonist treatment will block any effects of a self-administered opiate, discouraging further drug use. Counseling is important to help addicts identify their ―triggers‖ and develop a behavioral response to the cues to prevent relapse.

Textbook Reference: Treatment Programs for Opioid Use Disorder

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64. For the opiate addict, what are the advantages of buprenorphine maintenance compared to methadone?

Answer: Buprenorphine has weaker opioid effects so it is less likely to cause respiratory depression or result in overdose. Its longer duration of action means mild withdrawal symptoms on abstinence and fewer required clinic visits. A physician can prescribe it even if the office is not part of a federally regulated program, and the drug abuser can get a supply of buprenorphine because it produces only mild euphoria. The availability of an implantable option lasting six months makes compliance easier and pills can’t be lost or stolen. Finally, neonatal outcomes are better with buprenorphine and neonatal withdrawal symptoms are milder.

Textbook Reference: Treatment Programs for Opioid Use Disorder

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Test Bank to accompany

Psychopharmacology, Third Edition Meyer • Quenzer

Chapter 12: Psychomotor Stimulants: Cocaine and the Amphetamines Multiple Choice 1. Which statement does not describe cocaine? a. It is a psychomotor stimulant. b. It is an alkaloid that comes from the leaves of a bush. c. Coca chewing is no longer practiced in South America. d. It has been used in religious and ceremonial rituals.

Answer: c Textbook Reference: Cocaine: Background and History 2. Which statement regarding cocaine’s status in the late 1800s is false? a. Freud wrote an essay, Über Coca, warning people about the dangers of cocaine. b. Cocaine was being used as a treatment for morphine addiction and teething pain. c. Cocaine was an ingredient of beverages like Vin Mariani and Coca Cola. d. Cocaine abuse was becoming widespread throughout the population.

Answer: a Textbook Reference: Cocaine: Background and History 3. Cocaine use in the twentieth century a. was prohibited in over-the-counter medicines by the Harrison Narcotic Act. b. was ignored by government officials who considered marijuana to be ―public enemy number one.‖ c. involved administration via injection, snorting, or smoking. d. Both a and c Answer: d Textbook Reference: Cocaine: Background and History 4. Freebasing a. is the procedure used to derive crack cocaine for smoking. b. is especially dangerous because the ether used to extract the cocaine is highly flammable. c. results in a paste that is 80% cocaine. d. requires that baking soda be mixed with the cocaine during the extraction process.

Answer: b Textbook Reference: Basic Pharmacology of Cocaine 5. Which statement about cocaine administration and absorption is false?

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a. The cocaine metabolite benzoylecgonine can be detected for only a few hours after the last dose of drug. b. Rapid absorption occurs with intravenous and smoked forms of cocaine. c. Cocaethylene is a metabolite of cocaine and alcohol that exerts an effect similar to cocaine, but that lasts for a longer time. d. Smoking crack cocaine is addictive because the brain receives a large surge of drug, even though its effects don’t last very long.

Answer: a Textbook Reference: Basic Pharmacology of Cocaine 6. Cocaine acts in the nervous system by blocking a. monoamine transporters; voltage-gated potassium b. monoamine release; voltage-gated calcium c. monoamine transporters; voltage-gated sodium d. monoamine synthesis; voltage-gated calcium Answer: c Textbook Reference: Mechanisms of Cocaine Action

and

channels.

7. Which of the following is not an effect of low to moderate doses of cocaine? a. Amplification of both euphoria and dysphoria b. Mild anorexia c. Insomnia d. Incoherent speech Answer: d Textbook Reference: Acute Behavioral and Psyciological Effects of Cocaine 8. Chronic, high dose use of psychostimulants can lead to all of the following effects except a. irritability and anxiety. b. increased sexual interest. c. delusions. d. violence.

Answer: b Textbook Reference: Acute Behavioral and Psyciological Effects of Cocaine 9. Which of the following is a sympathomimetic effect of cocaine? a. Vasoconstriction b. Decreased heart rate c. Hypothermia d. Hypotension Answer: a Textbook Reference: Acute Behavioral and Psyciological Effects of Cocaine 10. A serious effect of heavy cocaine use, that might even be fatal, is a. stroke. b. heart failure.

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c. intracranial hemorrhage. d. All of the above Answer: d Textbook Reference: Acute Behavioral and Psyciological Effects of Cocaine 11. Psychostimulant injections a. increase stereotyped behavior when microinjected into the nucleus accumbens. b. increase locomotor behavior when microinjected into the striatum. c. have their reinforcing effects effectively blocked by 6-OHDA lesions of the nucleus accumbens. d. of amphetamine into the nucleus accumbens do not appear to be rewarding to animals, as they will not self-administer the drug.

Answer: c Textbook Reference: Acute Behavioral and Psyciological Effects of Cocaine 12. Lack of cocaine self-administration by mutant mice expressing a cocaine-insensitive dopamine transporter tells us that a. dopamine is not important for cocaine’s reinforcing effects. b. blockade of the dopamine transporter plays a key role in the reinforcing action of cocaine. c. the mutant dopamine transporter is unable to take up dopamine from the synaptic cleft. d. these mutant mice are able to experience cocaine reward but not cocaine reinforcement.

Answer: b Textbook Reference: Acute Behavioral and Psyciological Effects of Cocaine 13. Which statement about high cocaine responding (HCR) and low cocaine responding (LCR) rats is true? a. HCR and LCR rats differ in their responses to cocaine despite being genetically identical. b. LCR rats express more dopamine transporters in the nucleus accumbens and dorsal striatum than HCR rats. c. HCR rats show greater levels of extracellular dopamine than LCR rats, under drug-free conditions. d. When the animals are given a moderate dose of cocaine, extracellular dopamine levels increase more in the LCR rats than in the HCR rats.

Answer: b Textbook Reference: Acute Behavioral and Psyciological Effects of Cocaine 14. What technique has allowed researchers to study the effects of psychostimulants on measures like DAT occupancy in the living human brain? a. MRI b. CT c. EEG d. PET Answer: d

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Textbook Reference: Acute Behavioral and Psyciological Effects of Cocaine 15. Which factor is not important for determining the drug user’s ―high,‖ according to imaging studies? a. The number of dopamine transporters that are occupied by the drug b. The route of administration of the drug c. The baseline level of dopamine in the mesolimbic pathway d. The age of the user Answer: d Textbook Reference: Acute Behavioral and Psyciological Effects of Cocaine 16. What is the minimum dopamine transporter (DAT) occupancy required to achieve a ―high‖ from either cocaine or methylphenidate, based on imaging studies? a. 20–40% b. 40–60% c. 60–80% d. This has not been estimated due to individual variability.

Answer: b Textbook Reference: Acute Behavioral and Psyciological Effects of Cocaine 17. Which condition will produce the greatest psychostimulant effect, based on dopamine transporter (DAT) occupancy? a. Intranasal administration of drug b. 30% of transporters affected by drug c. IV administration of drug d. Low baseline of dopamine in the mesolimbic tract Answer: c Textbook Reference: Acute Behavioral and Psyciological Effects of Cocaine 18. Which statement concerning the receptor subtypes involved in psychostimulant effects is true? a. The locomotor-stimulating effects of cocaine involve the D5 receptor. b. D2 receptors are required for cocaine self-administration. c. Pimozide, a D 2 receptor blocker, completely eliminates amphetamine-induced euphoria. d. D1 receptor knockout mice are insensitive to both the locomotor stimulating and reinforcing effects of cocaine.

Answer: d Textbook Reference: Acute Behavioral and Psyciological Effects of Cocaine 19. Which of the following statements about early cocaine use is false? a. Cocaine use typically begins as early as age 10. b. Most users experiment with legal drugs such as alcohol before using cocaine. c. Cocaine is often used as a way to reduce anxiety or depression. d. The most common route for beginning users is intranasal administration.

Answer: a

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Textbook Reference: Cocaine Abuse and the Effects of Chronic Cocaine Exposure 20. Which of the following is not an important factor in maintaining cocaine use? a. Powerful stimulation effects of the drug b. Lack of a withdrawal syndrome c. Social reinforcement from friends d. Switch to smoking or IV routes of administration Answer: b Textbook Reference: Cocaine Abuse and the Effects of Chronic Cocaine Exposure 21. Cocaine binges a. result in a period of exhaustion, depression, and cravings. b. may involve use of up to 1500 grams of cocaine. c. do not produce an abstinence syndrome. d. typically last a week or longer.

Answer: a Textbook Reference: Cocaine Abuse and the Effects of Chronic Cocaine Exposure 22. Cocaine and in the dorsal striatum can be produced in cocainedependent individuals by exposure to videos of cocaine-related cues. a. ―high‖; increased D1 receptor binding b. tolerance; release of glutamate c. craving; release of dopamine d. relapse; increased D1 receptor binding Answer: c Textbook Reference: Cocaine Abuse and the Effects of Chronic Cocaine Exposure 23. Repeated exposure to cocaine and other psychostimulants a. can cause behavioral tolerance but not sensitization. b. can cause behavioral sensitization but not tolerance. c. can cause either behavioral tolerance or sensitization, depending on the pattern of exposure. d. causes neither behavioral tolerance nor sensitization.

Answer: c Textbook Reference: Cocaine Abuse and the Effects of Chronic Cocaine Exposure 24. Which statement about sensitization to psychostimulants is false? a. It can be divided into two phases—induction and expression. b. Its expression involves enhanced dopamine activity in the VTA → nucleus accumbens pathway. c. Glutamate from the medial prefrontal cortex plays a role. d. It results from continuous drug infusion.

Answer: d Textbook Reference: Cocaine Abuse and the Effects of Chronic Cocaine Exposure

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25. Long-access (6 hours per day) cocaine self-administration by rats has been shown to cause a. behavioral tolerance to the drug. b. reduced stimulation-evoked dopamine release in the nucleus accumbens. c. up-regulation of postsynaptic dopamine receptors. d. Both a and b Answer: d Textbook Reference: Cocaine Abuse and the Effects of Chronic Cocaine Exposure 26. Brain imaging studies of cocaine-abusing or -dependent individuals have found a. reduced methylphenidate-induced dopamine release in the dorsal striatum compared to controls (non cocaine–using individuals). b. damage to the striatum caused by repeated cocaine exposure. c. increased baseline D 2 receptor binding. d. Both a and c Answer: a Textbook Reference: Cocaine Abuse and the Effects of Chronic Cocaine Exposure 27. Which statement about cocaine abuse/dependence and cognitive function is true? a. Despite their compulsive drug use, people diagnosed with cocaine abuse or dependence do not show significant abnormalities on standard tests of cognitive function. b. Any cognitive deficits observed in cocaine abusing/dependent individuals must have been caused by their drug use, since numerous longitudinal studies have demonstrated that these individuals had normal cognitive function prior to the onset of drug use. c. Some abnormalities in cognitive function have been related to reduced gray matter volume of specific brain areas, based on MRI studies. d. Loss of white matter is the most important effect of cocaine that results in cognitive deficits.

Answer: c Textbook Reference: Cocaine Abuse and the Effects of Chronic Cocaine Exposure 28. Chronic or high dose cocaine use can cause all of the following except a. damage to somatosensory systems. b. a stroke. c. psychosis. d. perforation of the nasal septum.

Answer: a Textbook Reference: Cocaine Abuse and the Effects of Chronic Cocaine Exposure 29. Which statement about pharmacotherapy for cocaine dependence is false? a. Over 100 blinded placebo-controlled clinical trials have already been conducted to test medications against cocaine dependence. b. The FDA has approved several effective medications that have been shown to help people overcome their cocaine dependence. c. Many drugs that have been tested as potential therapeutic agents for cocaine dependence target some aspect of the dopamine system.

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d. Dopamine is not the only neurotransmitter system that has been targeted in the search for cocaine medications.

Answer: b Textbook Reference: Cocaine Abuse and the Effects of Chronic Cocaine Exposure 30. Vaccines against cocaine a. have not been effective in producing significant reductions in cocaine-induced behavior in animal studies. b. have not been tested in humans. c. could act by creating antibodies that bind the cocaine molecules, reducing the amount of drug that crosses the blood–brain barrier. d. may create antibodies that break down in the blood stream, causing long-term toxic side effects.

Answer: c Textbook Reference: Cocaine Abuse and the Effects of Chronic Cocaine Exposure 31. The approach of a contingency management program involves reducing while increasing _, and is based on the idea that drug-taking is an operant response. a. drug-associated reinforcement; nondrug reinforcers b. nondrug reinforcers; pharmacotherapeutic use c. relapse; self-esteem d. high-risk situations; coping strategies Answer: a Textbook Reference: Cocaine Abuse and the Effects of Chronic Cocaine Exposure 32. Amphetamine and related psychostimulants in the amphetamine-like family a. are drugs of abuse with no therapeutic value. b. resemble the neurotransmitter DA in their chemical structure. c. are all synthetic. d. are drugs of the twentieth century, having no use prior to 1900.

Answer: b Textbook Reference: The Amphetamines: Background and History 33. Ephedra a. is a safe and top-selling herbal remedy, also known as ―ma huang.‖ b. was banned by the FDA after many adverse reactions were reported. c. has no effect on appetite or weight, in spite of advertisers’ claims. d. has dangerous effects on the parasympathetic nervous system.

Answer: b Textbook Reference: The Amphetamines: Background and History 34. In which situation has amphetamine not been used medically and/or legally? a. Medication in early inhalers b. Means of staying awake on duty, by military personnel c. Treatment for ADHD

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d. Treatment of insomnia Answer: d Textbook Reference: The Amphetamines: Background and History 35. How is amphetamine different from methamphetamine? a. Amphetamine is metabolized quickly, whereas methamphetamine is degraded slowly. b. Methamphetamine users frequently go on binges or ―runs‖ of IV use; this is rare with amphetamine users. c. A form of methamphetamine can be taken by smoking. d. Methamphetamine is much more expensive to make than amphetamine.

Answer: c Textbook Reference: Basic Pharmacology of the Amphetamines 36. Amphetamine and methamphetamine affect synaptic transmission by a. increasing catecholamine reuptake. b. increasing metabolism by MAO. c. releasing dopamine from vesicles into the cytoplasm and from the cytoplasm into the extracellular fluid. d. shutting down the dopamine transporter and releasing dopamine back into the cytoplasm.

Answer: c Textbook Reference: Mechanisms of Amphetamine and Methamphetamine Action 37. Amphetamines increase catecholamine release in part by a. increasing calcium influx. b. reversing the transporter. c. increasing the firing rate of catecholamine neurons. d. decreasing autoreceptor function.

Answer: b Textbook Reference: Mechanisms of Amphetamine and Methamphetamine Action 38. Based on information from worldwide drug seizures, which class of abused drugs has increased the most from 1998 to 2014? a. Cannabis b. Cocaine, including crack cocaine and cocaine base c. Heroin and other opiate drugs d. Amphetamine-type stimulants Answer: d Textbook Reference: Behavioral and Neural Effects of Amphetamines 39. High-dose methamphetamine exposure has been linked to all of the following except a. cell death of noradrenergic neurons in the locus coeruleus. b. reduced striatal dopamine levels in chronic users of the drug. c. decreased staining tyrosine hydroxylase immunoreactive fibers in the dorsal striatum of mice.

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d. reduced dopamine transporter binding in both experimental animals and in human methamphetamine users.

Answer: a Textbook Reference: Behavioral and Neural Effects of Amphetamines 40. Chronic methamphetamine use has been associated with all of the following except a. psychosis and flashbacks. b. enhanced cognition. c. increased risk of stroke and myocardial infarction. d. premature aging.

Answer: b Textbook Reference: Behavioral and Neural Effects of Amphetamines 41. All of the following are symptoms of ADHD except a. high anxiety level. b. impulsivity. c. disruptive and unruly behavior. d. hyperkinesis.

Answer: a Textbook Reference: Methylphenidate 42. Which statement concerning the drugs used to treat ADHD is true? a. Side effects of these medications have not been of great concern to physicians. b. Low doses of these medications increase activity and arousal in children but not adults. c. Most of these drugs affect dopamine, with the exception of new drug Strattera that works by affecting norepinephrine. d. These drugs are safe to you because they have no abuse potential.

Answer: c Textbook Reference: Methylphenidate 43. Which of the following is not a drug used to treat ADHD? a. Ritalin b. Ephedrine c. Vyvanse d. Strattera Answer: b Textbook Reference: Methylphenidate 44. Some researchers have hypothesized that optimal prefrontal cortical (PFC) functioning and cognitive performance occur with activation of adrenergic receptors and DA receptors in the PFC. a. moderate; α2A; D1 b. maximum; α1 ; D2 c. maximum; α2A; D1 d. moderate; α1 ; D 2 Answer: a

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Textbook Reference: Methylphenidate 45. Modafinil is primarily used therapeutically for the treatment of a. ADHD. b. clinical depression. c. insomnia. d. narcolepsy.

Answer: d Textbook Reference: Modafinil 46. Mephedrone, methylone, MDPV, and α-PVP are all members of the class of a. methamphetamine-like compounds. b. drugs used to treat ADHD. c. naturally occurring psychostimulants. d. synthetic cathinones.

Answer: d Textbook Reference: Synthetic Cathinones 47. Which statement regarding mephedrone is false? a. It has been banned by the DEA. b. Despite its ability to produce a ―high‖ in human users, it lacks rewarding and reinforcing properties in experimental animals. c. It acts like amphetamine by releasing dopamine, norepinephrine, and serotonin from their respective nerve terminals. d. Two of the routes by which it is taken are snorting and oral ingestion.

Answer: b Textbook Reference: Synthetic Cathinones

Short Answer/Essay 48. Describe the historical use of cocaine in its natural form (chewing leaves), in beverages, and as treatments for various ailments. How did cocaine use change in the twentieth century?

Answer: For several thousand years, cocaine has been taken by the inhabitants of cocagrowing regions by chewing coca leaves. After cocaine was purified in the nineteenth century it began to be consumed orally in the form of Vin Mariani, other beverages like Coca-Cola, and in medications to treat numerous ailments. From the 1920s to the 1960s, cocaine was initially used primarily among avant-garde artists and performers, but beginning in the 1970s the United States experienced an escalation of cocaine use, first by snorting or IV injection and then later by smoking crack cocaine.

Textbook Reference: Cocaine: Background and History 49. Identify the various routes of administration for cocaine. What routes of administration yield the most rapid absorption of cocaine? Identify two metabolites of

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cocaine use; one found after use of cocaine alone and the other found after using a combination cocaine and alcohol.

Answer: Cocaine may be taken orally, intranasally, by IV injection, or by smoking. The most rapid absorption occurs following IV injection and smoking. Two cocaine metabolites are benzoylecgonine (cocaine alone) and cocaethylene (cocaine plus alcohol).

Textbook Reference: Basic Pharmacology of Cocaine 50. Describe the effects of cocaine at the synapse in detail. What specific effects are most important for cocaine’s reinforcing and addictive characteristics? What effects of cocaine are responsible for its action as a local anesthetic?

Answer: Cocaine blocks the membrane transporters for dopamine, norepinephrine, and serotonin, thus preventing reuptake and increasing synaptic transmission for all three of these neurotransmitters. Blockade of dopamine reuptake and resulting increase in dopamine transmission are most important for cocaine’s reinforcing and addictive characteristics. Blocking of voltage-gated sodium channels is responsible for cocaine’s action as a local anesthetic.

Textbook Reference: Mechanisms of Cocaine Action 51. List several effects of cocaine that occur at low to moderate doses. Which of these effects are considered to be part of the cocaine ―high‖? Identify several aversive effects that occur in high dose users.

Answer: Effects of low to moderate doses include mood amplification (both euphoria and dysphoria), heightened energy, sleep disturbance, motor excitement, talkativeness, hyperactive ideation, increased sexual interest, anger/verbal aggression, mild to moderate anorexia, and inflated self-esteem. The cocaine ―high‖ includes feelings of exhilaration and euphoria, a sense of well-being, enhanced alertness, heightened energy/diminished fatigue, and self-confidence. Aversive effects in high dose users include irritability, exhaustion, insomnia, compulsive motor stereotypies, incoherent speech, disjointed flight of ideas, decreased sexual interest, extreme violence, total anorexia, and delusions of grandiosity.

Textbook Reference: Acute Behavioral and Psyciological Effects of Cocaine 52. Cocaine is considered to be a sympathomimetic drug. What does that mean, and what are some of the sympathomimetic effects of this compound?

Answer: A sympathomimetic drug is one that produces symptoms of sympathetic nervous system activation. Cocaine’s sympathomimetic effects consist of tachycardia (increased heart rate), vasoconstriction, hypertension, and hyperthermia.

Textbook Reference: Acute Behavioral and Psyciological Effects of Cocaine 53. What have knockout studies and research with receptor agonists/antagonists contributed to the understanding of the role of dopamine in the behavioral and reinforcing effects of psychostimulants?

Answer: The mesolimbic dopamine pathway from the VTA to the nucleus accumbens plays a key role in psychostimulant-induced locomotor behavior and reinforcement in laboratory animals. The nigrostriatal dopamine pathway from the substantia nigra to the

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dorsal striatum plays a key role in psychostimulant-induced stereotyped behaviors in laboratory animals.

Textbook Reference: Acute Behavioral and Psyciological Effects of Cocaine 54. Research has shown that some laboratory rats respond strongly to a moderate dose of cocaine (high responders; HCR), whereas other rats respond more weakly (low responders; LCR). What is the underlying neurochemical basis for this difference?

Answer: Compared to HCR rats, LCR rats express more dopamine transporters in the nucleus accumbens and dorsal striatum. As a result, a moderate dose of cocaine causes a larger increase in extracellular dopamine levels in the HCR rats, which leads to greater dopaminergic signaling and activation of locomotor behavior Textbook Reference: Acute Behavioral and Psyciological Effects of Cocaine 55. According to imaging studies of human brains, what three factors influence the occurrence and intensity of a cocaine or methylphenidate ―high‖?

Answer: The three factors are the baseline level of dopamine activity in the mesolimbic pathway; the amount of dopamine transporter occupancy produced by the drug; and the rate at which transporter occupancy occurs, which depends on the route of drug administration.

Textbook Reference: Acute Behavioral and Psyciological Effects of Cocaine 56. Which dopamine receptor subtype is most important for the functional effects of psychostimulants? What is the evidence for this conclusion?

Answer: The D 1 receptor is most important for the functional effects of psychostimulants, including locomotor stimulating and reinforcing effects. This conclusion is based especially on the results of knocking out different dopamine receptor subtypes in mice.

That is, D 1 knockout mice, but not mice with genetic disruption of other dopamine receptor subtypes, fail to respond to psychostimulants like cocaine, either with respect to locomotor activation or drug self-administration.

Textbook Reference: Acute Behavioral and Psyciological Effects of Cocaine 57. List several reasons why people initiate cocaine use, and then identify several reasons why these same individuals may not continue to experiment with cocaine to the point of abuse.

Answer: People may initiate cocaine use to satisfy their curiosity; facilitate social interactions; relieve feelings of depression, anxiety, or guilt; have fun and celebrate; or simply to get ―high.‖ Cocaine may not continue to the point of abuse because of druginduced anxiety, unavailability of the drug, cost, the social and legal consequences of illicit drug use, and fear of losing control over one’s drug-taking behavior.

Textbook Reference: Cocaine Abuse and the Effects of Chronic Cocaine Exposure 58. What factors contribute to an individual becoming a cocaine abuser? Describe the pattern of use that occurs during cocaine binges, and the abstinence syndrome that follows.

Answer: These factors include the stimulating, euphoric, and confidence-enhancing effects of the drug; positive social responses from friends; comorbidity with other

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psychiatric disorders; stress; and switching from intranasal use to crack smoking, freebasing, or IV injection. During a cocaine binge, the individual continues using the drug repeatedly until the supply runs out. The abstinence syndrome consists of three phases: crash, withdrawal, and extinction.

Textbook Reference: Cocaine Abuse and the Effects of Chronic Cocaine Exposure 59. What have brain imaging studies in humans and related animal model studies told us about the neurochemical mechanisms of cocaine craving?

Answer: These studies have shown that cocaine craving is associated with increased dopamine release in several brain areas, including the dorsal and ventral striatum, amygdala, hippocampus, and prefrontal cortex.

Textbook Reference: Cocaine Abuse and the Effects of Chronic Cocaine Exposure 60. Describe the difference between psychostimulant tolerance and sensitization, indicate what patterns of drug exposure cause one or the other to occur, and identify the two phases of sensitization.

Answer: Psychostimulant tolerance refers to a reduced responsiveness to the drug, whereas sensitization refers to an increased responsiveness to the drug. Continuous exposure causes tolerance, whereas intermittent exposure causes sensitization. The two phases of sensitization are induction and expression.

Textbook Reference: Cocaine Abuse and the Effects of Chronic Cocaine Exposure 61. What changes occur in the rat dopamine system under conditions of cocaine tolerance produced by long-access cocaine self-administration? Are brain imaging studies of cocaine abusing or dependent individuals consistent with the rat results?

Answer: In cocaine tolerance, there is reduced intracellular dopamine levels in the nucleus accumbens, reduced dopamine release, reduced baseline dopamine uptake, reduced ability of cocaine to inhibit dopamine uptake, and reduced sensitivity of dopamine autoreceptors. Brain imaging of people who are cocaine abusing or dependent have shown reduced sensitivity of the dopamine system to a methylphenidate challenge, which is consistent with the rat results.

Textbook Reference: Cocaine Abuse and the Effects of Chronic Cocaine Exposure 62. Describe the serious neurological consequences of chronic or high dose cocaine use as well as the effects of such use on other systems of the body.

Answer: Neurological consequences can include stroke, seizures, panic attacks, paranoid psychosis, and hallucinations such as ―cocaine bugs.‖ Effects on other body systems include cardiac problems (e.g., arrhythmias, myopathy, or myocardial infarction); disorders of the lungs, gastrointestinal system, liver, and kidneys; perforation of the nasal septum due to cocaine snorting; and HIV/AIDS from IV injection with dirty needles.

Textbook Reference: Cocaine Abuse and the Effects of Chronic Cocaine Exposure 63. Describe how behavioral treatment programs based on operant conditioning principles are designed to reduce cocaine abuse.

Answer: Such programs are based on the premise that drug taking is an operant response that persists mainly as a result of the reinforcing properties of the drug. The program aims

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to reduce drug-associated reinforcement and to increase the availability of nondrug reinforcers. One such program is the contingency management program, which reinforces negative urine tests with vouchers that can be exchanged for local retail items.

Textbook Reference: Cocaine Abuse and the Effects of Chronic Cocaine Exposure 64. List several members of the amphetamine family of drugs. What do they have in common structurally? Identify two such compounds that occur in nature. How have amphetamines been used to treat diseases and enhance daily functioning, prior to being restricted by the government?

Answer: Members of the amphetamine family include amphetamine, methamphetamine, cathinone, and ephedrine. They are all structurally related to dopamine. Cathinone and ephedrine occur in nature. Historically, members of the amphetamine family have been used for weight loss, treatment of asthma (as a constituent of inhalers), treatment of narcolepsy, and to maintain alertness (e.g., by military personnel and students).

Textbook Reference: The Amphetamines: Background and History 65. Compare methamphetamine with amphetamine in terms of route of administration, potency, effects at the synapse, psychological effects, and neurotoxicity.

Answer: Amphetamine is usually taken orally or by IV or subcutaneous injection.

Methamphetamine can be taken orally, snorted, injected intravenously, or smoked.

Methamphetamine is much more potent than amphetamine, but the synaptic effects are similar. Both drugs release dopamine and norepinephrine and block the reuptake of these catecholamines. Psychologically, both drugs cause euphoria, heightened alertness, and reduced fatigue, but methamphetamine use is more likely to lead to dependence than amphetamine use. Methamphetamine also has greater risk of producing neurotoxicity characterized by loss of dopaminergic axons and terminals in laboratory animals and by reduced striatal dopamine levels, dopamine transporter binding, and D 2 /D 3 receptor binding in chronic methamphetamine users compared to nonusers.

Textbook Reference: Behavioral and Neural Effects of Amphetamines 66. Describe the neurochemical effects of methylphenidate. Based on these effects, is methylphenidate more similar to cocaine or to amphetamine in its mechanism of action?

Answer: Methylphenidate binds to the dopamine and norepinephrine transporters, thereby blocking the reuptake of both neurotransmitters. This mechanism of action is more similar to cocaine than to amphetamine.

Textbook Reference: Methylphenidate 67. Briefly describe the symptoms of ADHD in children, the three different subtypes of ADHD, and how the symptoms of this disorder are altered by psychostimulant medications. Identify some of the concerns that have been raised with respect to longterm treatment of children with psychostimulants.

Answer: The major symptoms of ADHD are extreme inattentiveness, impulsivity, and hyperkinesis. Three subtypes are predominantly inattentive, predominantly hyperactiveimpulsive, and combined subtype. At low doses, psychostimulant medications paradoxically have calming effect on most children diagnosed with ADHD. The major concerns around long-term treatment of children with psychostimulants involve the

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possibility of reduced growth, drug-induced increases in heart rate and blood pressure, possible increase in the risk for developing tic disorders, possible risk of long-term effects on brain function (based mainly on animal studies), and the abuse potential of psychostimulants.

Textbook Reference: Methylphenidate 68. List a few drugs used in the treatment of ADHD that act selectively on the noradrenergic system. For each drug, indicate its mechanism of action on that system.

Based on these mechanisms, would you expect the noradrenergic-related medications to differ from traditional psychostimulant medications in their degree of abuse potential?

Answer: The drugs are atomoxetine, which is a selective inhibitor of the norepinephrine transporter, and clonidine and guanfacine, both of which are selective α2A-adrenergic receptor agonists. These drugs would be expected to have significantly less abuse potential than traditional psychostimulant medications used to treat ADHD. Textbook Reference: Methylphenidate 69. Describe the inverted U-shape function of catecholamine release/activity ascribed to the prefrontal cortex and cognitive functioning, and indicate how various ADHD medications can optimize this system.

Answer: Levels of catecholamine release are lowest under conditions of fatigue, intermediate under alert conditions, and highest under conditions of stress. At the lowest levels of release, there is too little NE and DA neurotransmission, and at the highest levels of release, there is excessive NE and DA transmission. In both cases, prefrontal cortex function and cognitive performance are less than optimal. Prefrontal cortex function and cognitive performance are the best at intermediate levels of catecholamine release due to optimal activation of α2A-adrenergic and D 1 dopamine receptors in this brain area. Some researchers have hypothesized with individuals with ADHD have deficient catecholamine activity in the prefrontal cortex, which can be reversed either by psychostimulants (which release catecholamines or block their reuptake) or by noradrenergic medications (which either block norepinephrine reuptake or directly activate α2A-adrenergic receptors).

Textbook Reference: Methylphenidate 70. Describe the behavioral and neurochemical effects of modafinil, and indicate the major therapeutic use of this drug.

Answer: Modafinil has behavioral stimulant and cognitive enhancing effects.

Neurochemically, it acts as a weak dopamine uptake inhibitor, and it additionally stimulates norepinephrine and orexin release and inhibits GABA release. Its major therapeutic use is in the treatment of excessive daytime sleepiness in people with narcolepsy, obstructive sleep apnea, and disordered sleep due to shift work.

Textbook Reference: Modafinil 71. List several members of the class of synthetic cathinones. How are these drugs typically consumed? Describe the two categories of synthetic cathinones based on their neurochemical mechanisms of action.

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Answer: Synthetic cathinones include mephedrone, methylone, MDPV, and α-PVP. These drugs are typically consumed by snorting and oral ingestion. The two categories of synthetic cathinones are amphetamine-like (which means that the drug stimulates the release of dopamine, norepinephrine, and serotonin) and cocaine/methylphenidate-like (which means that the drug blocks the reuptake of dopamine and norepinephrine).

Textbook Reference: Synthetic Cathinones 72. Describe the adverse effects of high doses of synthetic cathinones.

Answer: High doses of these drugs can produce liver failure, kidney damage, rhabdomyolysis, abnormal blood clotting, and psychiatric reactions ranging from acute anxiety to psychotic reactions. Synthetic cathinone overdose can be fatal.

Textbook Reference: Synthetic Cathinones

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Test Bank to accompany

Psychopharmacology, Third Edition Meyer • Quenzer

Chapter 13: Nicotine and Caffeine Multiple Choice 1. Tobacco leaves a. were not cultivated in the New World until seeds were brought over by Columbus in 1492. b. come in a large and a small leaf form, the latter being used for most modern-day tobacco. c. can be smoked in pipes, chewed, or even snorted in a form called snuff. d. were processed into cigarettes in the early 1900s.

Answer: c Textbook Reference: Nicotine: Background and History 2. Nicotine a. makes up about 10% of the dry tobacco leaf. b. enters a smoker’s lungs on particles of tar. c. reaches the bloodstream from a typical cigarette in the amount of 6 to 11 mg. d. is one of many psychoactive substances in the tobacco leaf.

Answer: b Textbook Reference: Nicotine: Basic Pharmacology of Nicotine and Its Relationship to Smoking 3. What is the fastest way to administer nicotine to the brain? a. Intravenous route (IV) b. Snorting c. Smoking d. IV and smoking are equally fast Answer: c Textbook Reference: Nicotine: Basic Pharmacology of Nicotine and Its Relationship to Smoking 4. Which statement about the metabolism of nicotine is false? a. It yields the principal metabolite cotinine. b. All of the nicotine from a cigarette is metabolized in two hours. c. The liver enzyme CYP2A6 is involved. d. Inefficient metabolizers may be less likely to become cigarette smokers.

Answer: b Textbook Reference: Nicotine: Basic Pharmacology of Nicotine and Its Relationship to Smoking

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5. Nicotinic receptors a. are metabotropic receptors that bind acetylcholine. b. consist of three subunits: α, β, and γ. c. are constructed of subunits that form a potassium channel in the cell membrane. d. can become silenced by depolarization block with repeated stimulation.

Answer: d Textbook Reference: Nicotine: Mechanisms of Action 6. Studies of the behavioral and physiological effects of nicotine a. show that nicotine has a relaxing and calming effect in both smokers and nonsmokers. b. indicate that nicotine decreases reaction time in a visual information processing task in smokers but not in individuals who have never smoked. c. show that nicotine decreases errors of omission and increases attention in nonsmokers. d. suggest that the effects observed can be completely attributed to reversal of withdrawal symptoms in smokers asked to abstain for the duration of the study.

Answer: c Textbook Reference: Nicotine: Behavioral and Physiological Effects 7. Nicotine self-administration a. depends on the dopamine pathway to the nucleus accumbens for its reinforcing effects. b. is equal to amphetamine or cocaine self-administration in intensity. c. occurs at higher doses in adults than adolescents, according to animal studies. d. depends on the α4 subunit of the nicotinic receptor.

Answer: a Textbook Reference: Nicotine: Behavioral and Physiological Effects 8. Studies with knockout mice genetically engineered to lack particular nicotinic receptor subunits have shown that VTA nicotinic receptors with the and subunits are important for nicotine addiction. a. α6; β2 b. α5; α6 c. α4; α5 d. α5; β2 Answer: a Textbook Reference: Nicotine: Behavioral and Physiological Effects 9. Which of the following is not a physiological effect of nicotine? a. Release of norepinephrine and epinephrine b. Increased heart rate and elevated blood pressure c. Increased secretion of stomach acid and ulcer formation d. Decreased parasympathetic activity Answer: d Textbook Reference: Nicotine: Behavioral and Physiological Effects 10. Which statement about nicotine poisoning is false?

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a. It is frequently caused by smoking, because a pack of cigarettes contains several lethal doses. b. It has occurred in children who have accidentally consumed tobacco, from cigarette stubs left in ashtrays, for example. c. It is most likely caused by exposure to nicotine-based insecticides. d. It can cause death due to depolarization block of the breathing muscles.

Answer: a Textbook Reference: Nicotine: Behavioral and Physiological Effects 11. What role does nicotine play in the life and survival of the tobacco plant? a. Helps with photosynthesis b. Toxicity protects the plant from being eaten c. Provides help with energy storage d. Assists in pollination Answer: b Textbook Reference: Nicotine: Behavioral and Physiological Effects 12. Acute tolerance to nicotine a. takes place in the course of a single day. b. is different from short-term tolerance. c. does not affect the reinforcing effects of smoking. d. does not overlap chronic tolerance.

Answer: a Textbook Reference: Nicotine: Behavioral and Physiological Effects 13. The nicotine abstinence syndrome a. can be treated with the drug mecamylamine. b. results in increased locomotor activity in animals. c. is characterized by a decreased ability to experience rewarding stimuli. d. involves reduced dopamine in the nucleus accumbens.

Answer: c Textbook Reference: Nicotine: Behavioral and Physiological Effects 14. Which of the following is not a symptom of the nicotine abstinence syndrome? a. Weight loss b. Insomnia c. Trouble concentrating d. Restlessness Answer: a Textbook Reference: Nicotine: Behavioral and Physiological Effects 15. Which event did not reduce cigarette consumption to some degree? a. Cigarette taxes doubled. b. Antismoking ads appeared. c. Great Depression occurred. d. World War II began.

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Answer: d Textbook Reference: Nicotine: Cigarette Smoking and Vaping 16. With respect to the demographics of cigarette smoking, a. about 15% of the population over 18 years of age use e-cigarettes. b. approximately 50% of the population 12 and over smokes, according to a 2011 survey. c. about 80% of users of tobacco engage in their use via smoking cigarettes. d. smoking is positively correlated with education.

Answer: c Textbook Reference: Nicotine: Cigarette Smoking and Vaping 17. According to researchers, which of the following is not a reason adolescents smoke? a. To establish their independence b. To lose weight c. To be socially accepted by their peer group d. To defy parental wishes Answer: b Textbook Reference: Nicotine: Cigarette Smoking and Vaping 18. What is the difference between a regular smoker and an established smoker? a. A regular smoker smokes occasionally; an established smoker smokes daily. b. A regular smoker smokes on a regular basis, but not daily like an established smoker does. c. A regular smoker is not committed to smoking; an established smoker is dependent on nicotine. d. There is no difference between the two types of smokers.

Answer: b Textbook Reference: Nicotine: Cigarette Smoking and Vaping 19. Various models argue that smoking provides certain advantages to the smoker. Which of the following is not an example of such proposed advantage? a. Smoking allows the smoker greater mood control, specifically by controlling nicotine delivery. b. Smoking provides increased concentration for the smoker. c. Smoking allows the smoker a time of increased energy and activity. d. Smoking reduces the irritability and stress that occurs between cigarettes.

Answer: c Textbook Reference: Nicotine: Cigarette Smoking and Vaping 20. When smokers are given cigarettes lower in nicotine and tar, a. they reduce their intake slightly. b. there is no change in smoking behavior. c. there is a marked decrease in their smoking behavior. d. they smoke more.

Answer: d Textbook Reference: Nicotine: Cigarette Smoking and Vaping

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21. Which of the following is not an example of the benefits of nicotine gum? a. Ease of nicotine delivery b. Lack of side effects c. Over-the-counter (OTC) availability d. Rapid nicotine delivery Answer: b Textbook Reference: Nicotine: Cigarette Smoking and Vaping 22. ―Chippers‖ a. have been studied in the context of both nicotine and opiate use. b. have shown researchers that tolerance and dependence are not separate phenomena. c. do not develop either short-term or long-term tolerance. d. are individuals who smoke one or two cigarettes a week for at least a few years.

Answer: a Textbook Reference: Nicotine: Cigarette Smoking and Vaping 23. Which of the following is probably not important in maintaining smoking during the day? a. Avoidance of nicotine withdrawal symptoms b. Sensory aspects of smoking acting as secondary reinforcers of smoking through many past pairings with nicotine c. Enhanced release of dopamine in the nucleus accumbens with cigarette use d. The perceived pleasant qualities of cigarette smoke for the regular smoker Answer: c Textbook Reference: Nicotine: Cigarette Smoking and Vaping 24. Smoking is not an important contributing factor in a. seizures. b. cancer. c. cardiovascular disease. d. low birth weight in infants.

Answer: a Textbook Reference: Nicotine: Cigarette Smoking and Vaping 25. Which toxic substance is not produced or released during the smoking of tobacco? a. Tar b. Nicotine c. Nitrosamines d. Mecamylamine Answer: d Textbook Reference: Nicotine: Cigarette Smoking and Vaping 26. Which statement about quitting the smoking is true? a. The majority of smokers are not interested in giving up their smoking habit. b. Relatively few (<10%) smokers attempt to quit each year.

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c. Quitting the smoking habit is very difficult and requires many attempts. d. Placing warnings on cigarette packages and increasing cigarette taxes have had virtually no impact on usage or quitting rates.

Answer: c Textbook Reference: Nicotine: Cigarette Smoking and Vaping 27. Which formulation has not been used in nicotine replacement therapy? a. Lozenge b. Patch c. Nasal spray d. Pill Answer: d Textbook Reference: Nicotine: Cigarette Smoking and Vaping 28. Nicotine replacement therapy a. was first approved as a transdermal patch. b. should not be used in combination (e.g., inhaler plus patch). c. can be achieved by using mecamylamine. d. is generally very easy to use and in most cases allows for flexible, rapid dosing.

Answer: d Textbook Reference: Nicotine: Cigarette Smoking and Vaping 29. Which antidepressant is currently being used to help smokers withdraw from nicotine? a. Zoloft b. Paxil c. Zyban d. Prozac Answer: c Textbook Reference: Nicotine: Cigarette Smoking and Vaping 30. Which statement about caffeine is false? a. Tea contains both caffeine and theophylline, both stimulants. b. About 50% of adults consume caffeinated beverages. c. The average intake of caffeine in the United States is 200 to 400 mg per day. d. Children are avid consumers of caffeine in the form of soda and chocolate.

Answer: b Textbook Reference: Caffeine: Background 31. In addition to coffee and tea, caffeine is found in all of the following except for a. analgesic drugs. b. cough suppressants. c. OTC stimulants. d. diet soda.

Answer: b Textbook Reference: Caffeine: Background

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32. Caffeine a. is rapidly and completely absorbed through the gastrointestinal tract, primarily the small intestine. b. has a half-life that averages about eight hours. c. accumulates over the day, with significant amounts remaining in the blood stream the following morning. d. is metabolized more slowly in smokers.

Answer: a Textbook Reference: Caffeine: Basic Pharmacology of Caffeine 33. In laboratory animals, the effect of increasing doses of caffeine causes a. reduced activity, followed by increased activity. b. dose-dependent increases in activity. c. increased activity, followed by decreased activity. d. dose-dependent decreases in activity.

Answer: c Textbook Reference: Caffeine: Behavioral and Physiological Effects 34. Which of the following is not an effect of caffeine reported by regular users? a. Increased relaxation b. Self-confidence c. Improved mood d. More focused attention Answer: a Textbook Reference: Caffeine: Behavioral and Physiological Effects 35. An important medical use for caffeine is in the treatment of a. migraines. b. ADHD. c. diuresis. d. apnea.

Answer: d Textbook Reference: Caffeine: Behavioral and Physiological Effects 36. Which statement about people who are tolerant and/or dependent on caffeine in coffee is false? a. They are considered addicted to caffeine. b. They may develop a headache if they miss their morning cup of coffee. c. They may exhibit no trouble sleeping after consuming coffee right before bedtime. d. They may develop an intense craving for coffee if they try to stop drinking it.

Answer: a Textbook Reference: Caffeine: Behavioral and Physiological Effects 37. Caffeine withdrawal is characterized by a. headache.

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b. fatigue. c. impaired ability to concentrate. d. All of the above Answer: d Textbook Reference: Caffeine: Behavioral and Physiological Effects 38. Which of the following is not a characteristic of caffeine intoxication? a. Tachycardia (increased heart rate) b. Drowsiness c. Gastrointestinal upset d. Nervousness Answer: b Textbook Reference: Caffeine: Behavioral and Physiological Effects 39. Current evidence suggests that caffeine exerts its stimulant effects at the synapse by a. inhibiting cAMP phosphodiesterase. b. decreasing cyclic AMP levels. c. blocking adenosine receptors. d. blocking GABA A receptors.

Answer: c Textbook Reference: Caffeine: Mechanisms of Action 40. Which statement about adenosine is false? a. It is a constituent of ATP. b. It builds up during wakefulness, creating a state of drowsiness. c. It acts on four different receptor subtypes. d. It is released by caffeine.

Answer: d Textbook Reference: Caffeine: Mechanisms of Action 41. Caffeine’s antagonism of both and receptors, especially in the striatum, is important in the arousing and activating effects of the drug. a. A1 ; A2B b. A2A; A 2B c. A1 ; A2A d. A2A; A 3 Answer: c Textbook Reference: Caffeine: Mechanisms of Action 42. One potentially dangerous effect of the combination of energy drinks and alcohol is that a. children are likely to consume such drinks. b. alcohol-related impairment is still present although the individual may feel less intoxicated. c. energy drinks prevent the metabolism of alcohol. d. energy drinks enhance the absorption of alcohol.

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Answer: b Textbook Reference: Caffeine: Mechanisms of Action

Short Answer/Essay 43. Briefly describe the progression from cultivation of tobacco leaves in the New World to popularization and commercialization of the cigarette in twentieth-century America.

Answer: The history of cultivation goes back at least 5,000 years in South America.

Tobacco was unknown in Europe until the voyages of Columbus in the 1490s. Pipe smoking in Europe was popular as was snorting the tobacco powder. Colonist John Rolfe obtained a popular strain used in South America and was able to cultivate it in Virginia.

Cigarettes became popular in Europe and the United States in the mid -1800s, and mass production was introduced with the appearance of cigarette rolling machines.

Textbook Reference: Nicotine: Background and History 44. Describe the composition of a typical cigarette and explain how the psychoactive component is delivered to the body and brain. Where in the brain does nicotine exert its primary effects?

Answer: An average cigarette contains about 8 mg of nicotine, of which about 2 mg reaches the bloodstream when smoked. The nicotine is carried into the lungs along with hydrocarbons known as tar, which themselves contribute to the taste and smell of the smoke. Absorption into the blood is rapid, mediated via the large surface area of the lungs. Nicotine delivered this way actually reaches the brain quicker than an intravenous injection of nicotine (within 7 seconds). Each puff delivers an additional nicotine supply into the brain. Nicotine acts on widely distributed nicotinic receptors in the brain, including areas such as the cortex, hippocampus, striatum, thalamus, and ventral tegmentum.

Textbook Reference: Nicotine: Basic Pharmacology of Nicotine and Its Relationship to Smoking 45. Describe the effects of nicotine on mood in smokers and nonsmokers.

Answer: Smokers: calmness, relaxation (although some effects in smokers may be due to relief from withdrawal effects). Nonsmokers: arousal, tension, dizziness, nausea.

Textbook Reference: Nicotine: Behavioral and Physiological Effects 46. Describe the evidence, from both human and animal studies, that nicotine enhances cognitive function, and indicate which receptor subunits are important for various tasks.

Answer: Nicotine can improve performance in humans in attentional and memory tasks for both abstinent smokers and nonsmokers. Effects on attention in humans can be seen for those pre-screened as having a low attention trait. In rodents, nicotine improves performance in spatial learning tasks and contextual fear conditioning (which involves memory). Nicotinic receptors containing α4 and β2 subunits (high-affinity receptors) may be crucial for nicotine-induced cognitive enhancement.

Textbook Reference: Nicotine: Behavioral and Physiological Effects

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47. Discuss the role of dopamine and non-dopamine factors in the rewarding aspects of nicotine.

Answer: Nicotine increases burst firing of dopamine neurons in the pathway from the ventral tegmentum to the nucleus accumbens and also increases extracellular dopamine in the accumbens, as measured via microdialysis. Destruction of this dopamine pathway, using 6-hydroxydopamine, interferes with nicotine self-administration in rodents. Nondopamine influence may come about via nicotine-induced stimulation of the sympathetic nervous system, which produces a release of norepinephrine and epinephrine from the adrenal glands (adrenal medulla), which can produce an elevated feeling of arousal that could contribute to the reinforcing properties of nicotine.

Textbook Reference: Nicotine: Behavioral and Physiological Effects 48. Identify some physiological effects of nicotine that have the potential to cause longterm problems. What are the most likely conditions for nicotine poisoning? Is there any positive physiological benefit to smoking?

Answer: Increased sympathetic nervous system activity can contribute to an increase in blood pressure, and an increased risk of cardiovascular disease and stroke. This is in addition to increased risk of cancer (especially lung) and emphysema. Danger of nicotine poisoning can be associated with children eating cigarettes or gaining access to ecigarette cartridges, with farm workers coming in contact with wet tobacco leaves, and farm workers or others working in agriculture coming in contact with nicotine-containing insecticides. In terms of positive effects, it has been suggested that nicotine might be useful for lowering anxiety levels and possibly also depressive symptoms, and that some individuals with these disorders may be trying to self-medicate by self-administering nicotine via cigarette smoking.

Textbook Reference: Nicotine: Behavioral and Physiological Effects 49. Distinguish between short-term (acute) and long-term (chronic) tolerance in humans and explain how subunit composition of the receptors affect these. How can dependence and withdrawal be studied in animals?

Answer: Both acute and chronic tolerance may involve nicotinic receptor desensitization.

For acute tolerance, receptors with α4β2 subunits develop tolerance sooner that those with α7 subunits. On the other hand, the α4β2 receptors have a quicker recovery from tolerance. Chronic tolerance is associated with an increase in high affinity nicotinic receptor levels in the brain (perhaps to compensate for receptor desensitization?). In animals, one way to study the effects of chronic nicotine exposure is to make use of an osmotic minipump that will deliver a constant amount of nicotine over a 1- to 2-week period. The effects of loss of nicotinic stimulation can be studied by simply stopping the delivery of nicotine, or, for a quicker effect, administering a nicotinic receptor antagonist that can cross the blood–brain barrier, such as mecamylamine. Signs of nicotine withdrawal include shaking, teeth chatter, and increased startle response.

Textbook Reference: Nicotine: Behavioral and Physiological Effects 50. Describe the progression/stages in the development of a smoker, and indicate how the ―deprivation reversal model‖ plays a role.

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Answer: Several models have been proposed. One focuses on the progression of smoking with regard to the number of cigarettes smoked and the frequency. Another model emphasizes a progression from ―wanting‖ to ―craving‖ to ―needing‖ a cigarette. The ―deprivation reversal model‖ emphasizes the negative feelings produced in between smoking bouts, and the drive to alleviate these feelings by smoking again. These negative feelings include irritability, stress, and poor concentration. This could be viewed as a way to counter nicotine withdrawal effects.

Textbook Reference: Nicotine: Cigarette Smoking and Vaping 51. Cite evidence that shows that nicotine and non-nicotine factors are both important in maintaining smoking behavior. For example, discuss whether nicotine gum is completely successful in reversing withdrawal effects.

Answer: Other factors can contribute to maintaining smoking behavior. Sensory stimuli, for instance, such as the taste and smell of cigarettes can become part of a conditioned, positive response to smoking. Other components of cigarettes may also contribute, such as compounds that can inhibit monoamine oxidase and thereby possibly potentiate dopamine action in the brain. If other factors enter into the positive reinforcement from smoking cigarettes, nicotine gum alone may not relieve all of the withdrawal symptoms, and counseling may also play an important role.

Textbook Reference: Nicotine: Cigarette Smoking and Vaping 52. Discuss the advantages and disadvantages of the various nicotine replacement strategies. Then identify other pharmacological and behavioral interventions for treating tobacco dependence.

Answer: Nicotine gum and a nicotine patch can both provide nicotine without the other ingredients in tobacco smoke. The patch will give a more regular input of nicotine compared to the gum. These can be obtained over the counter, which makes them easier to obtain. Nicotine nasal spray and inhaler require a doctor’s prescription. The gum, spray, and inhaler approaches require frequent dosing. Sometimes these treatments can be combined. Bupropion (Zyban) can be prescribed, and may aid in smoking cessation via inhibition of dopamine and norepinephrine reuptake. Varenicline (Chantix) can also be prescribed, and acts as a partial agonist at nicotinic receptors in the brain. Efforts are also being made to develop a vaccine against nicotine. Counseling programs to help bring about behavioral modification are available to help treating tobacco dependence. Other efforts include health warnings about smoking and increased taxes on cigarettes.

Textbook Reference: Nicotine: Cigarette Smoking and Vaping 53. Describe the widespread availability and consumption of caffeine in the United States. How is it typically consumed, absorbed, and metabolized?

Answer: Caffeine is very widely consumed. In the United States, about 85% of the population over 2 years of age takes in at least one caffeinated drink per day. The average daily consumption is about 165 mg. Sources of caffeine include coffee, tea, sodas, and chocolates. Absorption is partly via the stomach and more significantly via the small intestine. The half-life is about 4 hours, and most of the caffeine is excreted in the urine as metabolites.

Textbook Reference: Caffeine: Basic Pharmacology of Caffeine

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54. Identify the biphasic effect of caffeine observed in animals. What effects do low to moderate doses of caffeine have on humans? What effects do high doses have?

Answer: In animals, caffeine at low doses produces an increase in motor activity, but this becomes a decrease at higher dosages. In humans, lower dosages produce positive feelings of well-being, increased alertness and arousal, and increased ability to concentrate. Higher doses (greater than 400 mg) produce tension, anxiety, and jitteriness.

Textbook Reference: Caffeine: Behavioral and Physiological Effects 55. Give examples that show that caffeine produces tolerance, dependence, and an abstinence syndrome.

Answer: Acute caffeine administration can cause an increase in blood pressure, diuresis, and an increase in catecholamine release from the adrenal medulla. These effects are significantly reduced with chronic caffeine usage, indicating tolerance. Dependence is associated with a strong desire to take the drug, and persistence in its use despite harmful consequences. The DSM-5 recommends further research with regard to whether caffeine dependence should be included as a disorder. Withdrawal effects include headache, lethargy, and difficulty in concentrating.

Textbook Reference: Caffeine: Behavioral and Physiological Effects 56. What leads to caffeine intoxication and why is it sometimes mistaken for an anxiety disorder?

Answer: Caffeine intoxication can occur with a very high level of caffeine intake (as high as 1000 mg), and is associated with nervousness, restlessness, insomnia, and tachycardia.

These symptoms resemble those seen in anxiety disorders.

Textbook Reference: Caffeine: Behavioral and Physiological Effects 57. Describe the mechanism of action of caffeine at the synapse, and explain why other possible synaptic models have been ruled out.

Answer: Current concepts regarding mechanism of caffeine action center upon blockade of adenosine receptors in the brain. The level of caffeine required to produce this blockade is consistent with the consumption of 1–2 cups of coffee. Other possible mechanisms, such as inhibition of phosphodiesterase metabolism of cyclic AMP or blockade of GABA A receptors, would appear to require a higher level of caffeine than normally consumed.

Textbook Reference: Caffeine: Mechanisms of Action 58. How might dopamine be involved in the action of caffeine?

Answer: There is evidence that adenosine activation of adenosine receptors can inhibit the action of dopamine on D2 receptors, lowering the arousal effects of dopamine.

Caffeine inhibits the binding of adenosine to adenosine receptors, thus freeing up the dopamine receptor to restore a state of arousal.

Textbook Reference: Caffeine: Mechanisms of Action

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Test Bank to accompany

Psychopharmacology, Third Edition Meyer • Quenzer

Chapter 14: Marijuana and the Cannabinoids Multiple Choice 1. Harry Anslinger a. was a former drug ―czar‖ appointed by Presid ent Bush. b. is the current director of the Office of National Drug Control Policy. c. was the first Commissioner of Narcotics. d. opposed the Marijuana Tax Act in 1937.

Answer: c Textbook Reference: Background and History of Cannabis and Marijuana 2. Which statement about the uses of marijuana is false? a. Hemp was originally grown in colonial America for its psychoactive properties. b. Hemp has important non-drug purposes, and is used in rope, cloth, and paper. c. Cannabis plants contain more than 60 cannabinoids, some with psychoactive properties that make the plant attractive as a drug. d. Religious use of marijuana dates back to ancient China and India.

Answer: a Textbook Reference: Background and History of Cannabis and Marijuana 3. Which of the following is not a form of marijuana or cannabis derivative? a. Hashish b. Sinsemilla c. Hash oil d. Anandamide Answer: d Textbook Reference: Background and History of Cannabis and Marijuana 4. The major psychoactive ingredient of the marijuana plant is a. cannabinol. b. ∆9-tetrahydrocannabinol. c. anandamide. d. ∆6-tetrahydrocannabinol.

Answer: b Textbook Reference: Background and History of Cannabis and Marijuana 5. The amount of active ingredient absorbed during marijuana smoking depends on all of the following except for the a. amount of plant material used.

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b. potency of the plant material used. c. psychological state of the user. d. volume of each ―puff‖ or inhalation.

Answer: c Textbook Reference: Basic Pharmacology of Marijuana 6. Oral administration of marijuana a. results in a shorter duration of action of the drug than smoking. b. yields low but consistent levels of drug in the body. c. leads to reduced blood levels due to first-pass metabolism and breakdown of the drug in the stomach. d. is an easy way to regulate the amount of drug entering the body.

Answer: c Textbook Reference: Basic Pharmacology of Marijuana 7. Which statement regarding the most prevalent CNS cannabinoid receptor is false? a. It was discovered in 1988 by two independent groups of researchers. b. It is an ionotropic receptor, currently designated CB1 . c. It plays a role in locomotor activity, coordination, and memory. d. It is expressed in the basal ganglia, cerebellum, hippocampus, and cortex.

Answer: b Textbook Reference: Mechanisms of Action is not a possible effect of cannabinoids on the CB1 receptor.

8. Inhibition of a. cAMP formation b. voltage sensitive Ca2+ channels c. the release of GABA d. K+ channel opening Answer: d Textbook Reference: Mechanisms of Action 9. Which drug is a CB1 antagonist? a. SR 1416 b. Rimonabant c. Nabilone d. WIN 55,212-2 Answer: b Textbook Reference: Mechanisms of Action 10. Which statement about the endocannabinoids is false? a. They are synthesized by FAAH. b. They include arachidonic derivatives such as 2-AG and anandamide. c. They are not stored in vesicles. d. They are synthesized and released when needed, probably in response to Ca2+.

Answer: a Textbook Reference: Mechanisms of Action

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11. Endocannabinoids contribute to retrograde signaling in the hippocampus by a. blocking the reuptake transporters. b. blocking CB1 autoreceptors on the presynaptic terminals. c. inhibiting Ca2+-mediated GABA release. d. activating the CB1 receptors and increasing GABA release.

Answer: c Textbook Reference: Mechanisms of Action 12. To study the role of the endogenous cannabinoids, scientists have used mice genetically engineered to and . a. lack these compounds; drugs that block CB1 receptors b. lack CB1 and CB2 receptors; drugs that block CB1 receptors c. overexpress CB1 receptors; drugs that prevent metabolism of these compounds d. overexpress these compounds; drugs that enhance synthesis of these compounds Answer: b Textbook Reference: Mechanisms of Action 13. Mice lacking CB1 receptors or normal mice treated with a CB1 antagonist a. show decreased sensitivity to pain. b. exhibit decreased food intake. c. show decreased anxiety-like behaviors d. show decreased conditioned fear responses.

Answer: b Textbook Reference: Mechanisms of Action 14. Which statement regarding the drug SR 141716A is false? a. It decreases appetite and may serve as an antobesity agent. b. It causes hyperalgesia. c. It reduces depressive-like behaviors. d. It acts as a cannabinoid antagonist.

Answer: c Textbook Reference: Mechanisms of Action 15. Cannabinoids could be used therapeutically to treat all of the following except a. neuropathic pain. b. mood disorders. c. nausea. d. obesity.

Answer: d Textbook Reference: Mechanisms of Action 16. Moreau is sometimes referred to as the ―father of psychopharmacology,‖ mainly because he a. introduced hashish to high society in nineteenth-century Paris. b. was responsible for founding the ―club of hashish eaters.‖

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c. was one of the first to study the possible relationship between hashish use and mental illness. d. was a researcher who studied drugs and personally experimented with hashish.

Answer: c Textbook Reference: Acute Behavioral and Physiological Effects of Cannabinoids 17. Which statement about the four stages that describe the subjective marijuana experience is false? a. The ―buzz‖ is characterized by lightheadedness and tingling. b. The ―high‖ is a period of euphoria, laughter, and disinhibition. c. During the ―high,‖ people are most likely to report changes in perceptions and time sense. d. When ―stoned,‖ people typically report being calm, relaxed, and in a dream-like state.

Answer: c Textbook Reference: Acute Behavioral and Physiological Effects of Cannabinoids 18. One of the most reliable physiological effects of cannabis use in humans is a. slowing of heart rate. b. decreased blood flow to the skin. c. faint pulse. d. increased hunger.

Answer: d Textbook Reference: Acute Behavioral and Physiological Effects of Cannabinoids 19. Which of the following is not an adverse reaction to marijuana? a. Anxiety or panic, especially in first time users b. Feelings of paranoia, with high doses c. Nausea and gastrointestinal upset d. Depression or dysphoria Answer: c Textbook Reference: Acute Behavioral and Physiological Effects of Cannabinoids 20. Concerning the time course of THC levels and route of administration, a. plasma levels of THC peak more rapidly following injection or smoking than oral administration of the drug. b. people smoking marijuana typically reach their peak THC levels before they finish the cigarette or joint. c. oral administration of THC produces low plasma levels that drop off quickly. d. at maximum THC intoxication after smoking, brain and plasma THC levels are equilibrated.

Answer: a Textbook Reference: Acute Behavioral and Physiological Effects of Cannabinoids 21. Human studies have shown that marijuana use produces deficits/decreases in all of the following except a. verbal memory tasks.

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b. appetite. c. psychomotor tasks, such as driving an automobile. d. reaction time tasks.

Answer: b Textbook Reference: Acute Behavioral and Physiological Effects of Cannabinoids 22. Marijuana-induced deficits in memory can be reduced by administration of a. cannabidiol (CBD). b. alcohol. c. 2-AG. d. anandamide.

Answer: a Textbook Reference: Acute Behavioral and Physiological Effects of Cannabinoids 23. Which of the following is not among the discoveries showing that cannabinoids are reinforcing? a. Regular marijuana users choose THC-containing cigarettes over placebo cigarettes with no THC. b. THC taken orally is preferred over a placebo capsule with no THC. c. Users reliably choose higher THC content cigarettes over those with a lower THC content. d. All animals tested reliably self-administer high doses of THC. Answer: d Textbook Reference: Acute Behavioral and Physiological Effects of Cannabinoids 24. Animal studies of the rewarding effects of cannabinoids have a. found that THC is aversive to all species tested. b. shown that animals will self-administer the synthetic drugs WIN 55,212-2 and SR 141716A. c. demonstrated the importance of using low THC doses and pre-exposure to the drug. d. found reinforcing effects of THC in the place conditioning task but not the self administration paradigm.

Answer: c Textbook Reference: Acute Behavioral and Physiological Effects of Cannabinoids 25. The reinforcing effects of THC are dependent on , and involve . a. CB2 receptors; decreased dopamine release in the nucleus accumbens b. μ-opioid receptors; decreased endocannabinoid release in the nucleus accumbens c. CB1 receptors; increased dopamine release in the nucleus accumbens d. κ-opioid receptors; increased glutamate release in the prefrontal cortex Answer: c Textbook Reference: Acute Behavioral and Physiological Effects of Cannabinoids 26. Marijuana appears to stimulate dopamine release in the nucleus accumbens via inhibition of release in the . a. glutamate; VTA

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b. GABA; VTA c. glutamate; substantia nigra d. GABA; substantia nigra Answer: b Textbook Reference: Acute Behavioral and Physiological Effects of Cannabinoids 27. Which statement concerning marijuana use in the United States is the most accurate? a. There has been a steep increase in new users of marijuana since 1995. b. The government’s policies and media campaigns have been very effective in reducing marijuana use. c. The typical age for initiating marijuana use is around 13, based on a representative longitudinal study. d. The prevalence of drug use, including marijuana use, declines with age.

Answer: d Textbook Reference: Cannabis Abuse and the Effects of Chronic Cannabis Exposure 28. According to research, which factor is most likely to encourage an individual to progress from occasional to heavy marijuana use? a. The person is a risk-taker. b. The person has nagging, over-involved parents. c. The person’s first experiences with marijuana were positive. d. The person has too many adult responsibilities.

Answer: c Textbook Reference: Cannabis Abuse and the Effects of Chronic Cannabis Exposure 29. Tolerance to THC a. is not well established in animals. b. is mainly due to metabolic tolerance in both humans and animals. c. occurs very slowly over a six week period. d. has been measured in terms of decreases in CB1 receptor densities.

Answer: d Textbook Reference: Cannabis Abuse and the Effects of Chronic Cannabis Exposure 30. All of the following are withdrawal symptoms observed following long-term heavy marijuana use except a. increased sleep. b. a depressed mood. c. aggression. d. decreased appetite.

Answer: a Textbook Reference: Cannabis Abuse and the Effects of Chronic Cannabis Exposure 31. What happens during precipitated withdrawal from cannabinoids in animal studies? a. The THC being administered is withdrawn. b. The CB1 antagonist SR 141716A is administered.

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c. The CB1 drugs WIN 55,212-2 and SR 141716A are administered at the same time to precipitate withdrawal. d. THC is stopped and SR 141716A is administered.

Answer: b Textbook Reference: Cannabis Abuse and the Effects of Chronic Cannabis Exposure 32. Which of the following is not an effect of precipitated withdrawal from cannabinoids? a. Hyperactivity b. Decreased grooming behavior c. Wet-dog shakes d. Scratching Answer: b Textbook Reference: Cannabis Abuse and the Effects of Chronic Cannabis Exposure 33. Neurochemical changes associated with a marijuana abstinence syndrome include a. increased DA firing in the VTA. b. increased CRF release in the amygdala. c. decreased DA firing in the substantia nigra. d. decreased CRF release in the central nucleus.

Answer: b Textbook Reference: Cannabis Abuse and the Effects of Chronic Cannabis Exposure 34. Which statement regarding treatment of cannabis dependence is false? a. It may include outpatient programs offering cognitive behavior therapy and relapse prevention therapy. b. It is much more successful than treatment of other drug dependence problems, with very little relapse. c. It can include pharmacotherapy with antidepressants and mood stabilizers. d. It could someday include the use of oral THC to moderate marijuana cravings.

Answer: b Textbook Reference: Cannabis Abuse and the Effects of Chronic Cannabis Exposure 35. The relationship between chronic marijuana use and educational achievement a. is most likely explained by the fact that marijuana causes cognitive deficits. b. is a correlational relationship that does not merit further study. c. may be explained by the social environment of marijuana users and their values concerning education. d. has only been measured in terms of absenteeism which probably reflects motivational variables more than academic factors.

Answer: c Textbook Reference: Cannabis Abuse and the Effects of Chronic Cannabis Exposure 36. Which of the following is not a characteristic of amotivational syndrome? a. Anxiety b. Lack of planning c. Decreased productivity

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d. Apathy Answer: a Textbook Reference: Cannabis Abuse and the Effects of Chronic Cannabis Exposure 37. Recent longitudinal cohort studies investigating the relationship between heavy marijuana use and risk for developing psychosis a. show that there is no relationship between the two. b. indicate that early, heavy use of marijuana decreases the risk of later psychosis. c. suggest that early, heavy marijuana use doubles the risk of later development of psychotic symptoms. d. cannot be taken seriously because of individual differences.

Answer: c Textbook Reference: Cannabis Abuse and the Effects of Chronic Cannabis Exposure 38. Recent imaging studies have demonstrated some evidence of abnormalities or alterations in several brain structures, including the and the . a. amygdala; nucleus accumbens b. hippocampus; prefrontal cortex c. hypothalamus; prefrontal cortex d. VTA; limbic system Answer: b Textbook Reference: Cannabis Abuse and the Effects of Chronic Cannabis Exposure 39. All of the following are effects that have been correlated with chronic use of marijuana except a. development of anxiety disorders. b. adverse cardiac effects. c. immune system suppression. d. damage to lung tissue.

Answer: a Textbook Reference: Cannabis Abuse and the Effects of Chronic Cannabis Exposure 40. Which health effect of chronic marijuana use is least substantiated? a. Increased risk of bronchitis b. Decreased resistance to viral infections c. Reduction in reproductive function d. Increased development of precancerous lung conditions Answer: b Textbook Reference: Cannabis Abuse and the Effects of Chronic Cannabis Exposure 41. Synthetic designer cannabinoids have been called a. ―Smack.‖ b. ―THC2.‖ c. ―CB2.‖ d. ―Spice.‖ Answer: d

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Textbook Reference: Cannabis Abuse and the Effects of Chronic Cannabis Exposure

Short Answer/Essay 42. Describe the historical use of marijuana as agricultural commodity, medicine, and recreational drug in the United States. What role did Anslinger and various regulatory policies have on this use?

Answer: Hemp use may go back at least 8000 years. It was used in colonial America to make items such as rope, cloth, and paper. In the United States the recreational use of smoking marijuana became popular in the early 1900s. Harry Anslinger was appointed as a commissionar of narcotics in the federal government in 1930, and waged a campaign against marijuana, claiming it was extremely dangerous. A Marijuana Tax Act was passed in 1937 to discourage marijuana usage.

Textbook Reference: Background and History of Cannabis and Marijuana 43. Distinguish between the various cannabis derivatives including marijuana, hashish, hash oil, and sinsemilla in terms of potency and route of administration.

Answer: Marijuana is composed of leaves, stems, and tops of the marijuana plant.

Smoking is the most common form of administration, but mixing with food for oral consumption is another route of administration. Potency can vary widely depending on the strain of the plant. Marijuana in which pollination (and seed production) has been prevented produces sinsemilla, which can increase the potency of the plant. Hashish is a resin containing a higher THC content than regular marijuana, and can be administered either via smoking or orally with food. A waxy residue can also be formed by a process known as dabbing, in which the marijuana is extracted with butane to produce a residue, sometimes called honey oil, with higher THC content than regular marijuana. This material can be heated (for example, with e-cigarette vaporizers) to produce vapors for inhalation.

Textbook Reference: Background and History of Cannabis and Marijuana 44. Describe the factors that influence the amount of THC that is absorbed during smoking and oral administration. Explain why it takes more than two weeks to completely eliminate THC metabolites from the body.

Answer: During smoking, marijuana vapors enter the lung. The effective dose and latency to onset of effects of smoked marijuana are influenced by puff volume, puff frequency, inhalation depth, and breath-hold duration. Smoked THC is quickly absorbed through the lungs, resulting in rapidly rising levels in the blood plasma of the smoker. After peak levels are reached, plasma THC concentrations begin to decline as a result of a combination of metabolism in the liver and accumulation of the drug in the body’s fat stores. Oral consumption of marijuana leads to prolonged but poor absorption of THC, resulting in low and variable plasma concentrations. Oral THC can be metabolized in the stomach and also in the liver via first-pass metabolism after being absorbed from the stomach. Some of the drug and fat-soluble metabolites are stored in fat tissue. The gradual movement of THC and fat-soluble metabolites back out of fat stores means that

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sensitive urine-screening tests for THC-COOH can detect the presence of this metabolite more than two weeks after a single marijuana use.

Textbook Reference: Basic Pharmacology of Marijuana 45. Describe the discovery of the cannabinoid receptor (CB1 ) by two independent research groups. Characterize the receptor in terms of its location in the CNS, its probable location within the synapse, and the cellular effects it is responsible for. Identify a CB 1 receptor antagonist that has been used to clarify the role of this receptor.

Answer: One set of studies showed cannabinoid binding to putative receptors in the brain.

Another set of studies showed the production of m-RNA that coded for a G-protein (metabotropic) receptor in the same brain areas that contained the cannabinoid binding.

Additional studies showed that this m-RNA did in fact code for a cannabinoid receptor (termed CB1 ). This receptor was found to be significantly expressed in the basal ganglia, cerebellum, hippocampus, and cerebral cortex. These receptors have significant representation on axon terminals, but can also be found on cell bodies and dendrties.

Cellular effects include inhibiting voltage-gated calcium channels, inhibiting production of cyclic AMP, and activation of potassium channels. Activation on nerve terminals can lead to inhibition of transmitter release from the target terminal. Rimonabant is a CB 1 cannabinoid receptor antagonist that has been utilized to demonstrate receptor-mediated effects of cannabinoids.

Textbook Reference: Mechanisms of Action 46. Identify the two substances that have been shown to act as endocannabinoids in the CNS. List several characteristics of these substances that make them different from more traditional endogenous transmitter substances like dopamine.

Answer: The first endogenous cannabinoid discovered was anandamide (AEA). The second was 2-AG. Both of these compounds contain arichidonic acid within their structure. Instead of being stored in synaptic vesicles before being released like traditional transmitters such as dopamine, these compounds are synthesized and released as needed. This is due to their high lipid solubility, which would make vesicular storage difficult.

Textbook Reference: Mechanisms of Action 47. Describe the role of endocannabinoids in retrograde signaling in the hippocampus. Be sure to include the role of intracellular Ca2+ in your answer.

Answer: An increase in intracellular calcium in postsynaptic dendrites, either via entry into the dendrites or release from internal stores, can stimulate endogenous cannabinoid formation. The cannabinoid can then travel across the synapse in a retrograde direction to the nerve terminal of a neuron terminating on the dendrite of the cannabinoid producing cell. This in turn could inhibit the release of transmitter from that incoming neuron. This could take place in the hippocampus to inhibit glutamate release, and in other brain regions as well.

Textbook Reference: Mechanisms of Action 48. Describe the evidence, from animal studies, that the endocannabinoids are involved in the extinction of learned fear responses.

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Answer: In rats and mice, an auditory stimulus precedes a foot shock. The animals learn to associate the auditory stimulus with the aversive foot shock, and will exhibit a fear response (freezing) with just the auditory stimulus. This response can be reversed (extinguished) if then the animals are given the auditory stimulus but no foot shock. This fear response extinction will be inhibited if the animals are given a cannabinoid CB 1 receptor antagonist, such as rimonabant, suggesting that cannabinoids are involved in extinction of learned fear responses.

Textbook Reference: Mechanisms of Action 49. Describe the subjective, behavioral, and physiological changes associated with the stages of marijuana use referred to as the ―buzz,‖ the ―high,‖ and being ―stoned.‖ Under what conditions are adverse reactions most likely to occur?

Answer: The initial buzz can be associated with a light-headed or dizzy feeling and a tingling sensation. Being high is associated with euphoric feelings, disinhibition, and a readiness to laugh. Being stoned is associated with a calm, dreamlike state. An altered auditory or visual input may be noticed, as well as a feeling that more time has passed than has actually occurred. Negative effects, such as agitation and paranoia, can also occur, especially in first-time users.

Textbook Reference: Acute Behavioral and Physiological Effects of Cannabinoids 50. Under what circumstances do humans show deficits in cognition and psychomotor performance following acute cannabinoid use?

Answer: Acute cannabinoid exposure has been found to impair episodic verbal memory and working memory. In addition to memory impairment, deficits in verbal learning, attention, inhibitory control, and psychomotor function (e.g., reaction time) have also been associated with acute cannabinoid exposure. The amount of prior marijuana use has been shown to influence the results on some cognitive tests, with heavier use reducing the adverse effects of acute cannabinoid exposure.

Textbook Reference: Acute Behavioral and Physiological Effects of Cannabinoids 51. What laboratory evidence do scientists have that humans find cannabinoids reinforcing? Why has it been somewhat more difficult to demonstrate that animals find cannabinoids rewarding? Describe the two typical behavioral paradigms that are used.

Answer: Regular marijuana users could discriminate THC-containing marijuana cigarettes from placebo cigarettes containing no THC, and all participants preferred the marijuana with THC when given a choice. Pure THC taken orally in capsule form was also preferred over a placebo. Marijuana preference related to THC content, as users selected marijuana with a higher 1.95% THC content over marijuana containing only 0.63% THC. Problems in demonstrating rewarding effects of THC could be related to the observation that THC is only a partial agonist at CB 1 receptors. Synthetic cannabinoids such as WIN 55,222-2, which is a full agonist, readily give a positive result in a place preference test and in lowering the threshold for electrical self-stimulation, both indicative of rewarding properties. Also, too high a dose of cannabinoid may be less likely to produce a rewarding effect.

Textbook Reference: Acute Behavioral and Physiological Effects of Cannabinoids

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52. Describe the neural mechanisms that underlie both the reinforcing and aversive aspects of cannabinoid administration.

Answer: Cannabinoids can increase the firing of dopamine neurons travelling from the ventral tegmentum to the nucleus accumbens, and also to increase dopamine release in the nucleus accumbens. This effect may be indirect, possibly via inhibition of GABA release in the ventral tegmentum, freeing up the dopamine neurons from GABA-mediated inhibition of firing rate.

Textbook Reference: Acute Behavioral and Physiological Effects of Cannabinoids 53. What evidence is there that marijuana use is a serious national problem that shows little sign of improving or being influenced by current drug control policies? What age group seems to be at the greatest risk for cannabis use?

Answer: Marijuana is the most widely used illicit drug in the United States. In 2016, more than 20 million Americans age 18 or older were current marijuana users. In addition, there were 1.6 million users between 12 and 17 years of age. Marijuana use typically occurs in adolescence and peaks during young adulthood. If individuals have not yet tried marijuana by their mid-20s, they are unlikely to begin at a later age. The peak age range for illicit drug use is 18–25 years of age.

Textbook Reference: Cannabis Abuse and the Effects of Chronic Cannabis Exposure 54. Identify several factors that may increase an adolescent’s likelihood of using marijuana in the first place, or progressing from initial to regular use.

Answer: Risk factors in the development of heavy marijuana use by adolescents include emotional problems in the family, heavy drug use in the household and/or by peers, dislike of school and poor school performance, and an early age of first use of marijuana.

Another important factor may be the degree to which the young person experiences positive reactions to his or her early use of cannabis.

Textbook Reference: Cannabis Abuse and the Effects of Chronic Cannabis Exposure 55. Describe the differences between the marijuana abstinence syndrome in humans and the precipitated withdrawal syndrome reported in animals. What neural systems seem tobe responsible for these behavioral changes?

Answer: Studies of abstinence in long-term heavy marijuana users have reported a number of withdrawal symptoms, including irritability, increased anxiety, depressed mood, sleep disturbances, heightened aggressiveness, and decreased appetite. Precipitated withdrawal in animals (using a CB 1 receptor antagonist) produces an abstinence syndrome characterized by tremors, wet-dog shakes, increased grooming behaviors (facial rubbing, licking, and scratching), ataxia, and hunched posture. These withdrawal symptoms are associated with a decrease in DA cell firing in the VTA and reduced DA release in the nucleus accumbens, increased corticotropin-releasing factor (CRF) release in the central nucleus of the amygdala, and increased secretion of stress hormones such as corticosterone.

Textbook Reference: Cannabis Abuse and the Effects of Chronic Cannabis Exposure

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56. Identify two pharmacological treatment approaches and two non-drug treatment approaches for addressing the problems of cannabis dependence. Why are most of these therapies not very successful?

Answer: Pharmacological approaches include the use of an opiate antagonist, such as naltrexone, and atomoxetine, a norepinephrine reuptake inhibitor. Non-drug approaches include cognitive behavioral therapy and relapse prevention training. Similar to other drug dependency programs, there is a high rate of relapse, possibly due to an altered brain state that is very susceptible to relapse because of persistent craving for the drug.

Textbook Reference: Cannabis Abuse and the Effects of Chronic Cannabis Exposure 57. Identify the known effects of chronic cannabis use on health. What areas need to be researched further?

Answer: Since cannabis is usually consumed by smoking, the possibility of lung damage is one area of concern. The risk of experiencing a myocardial infarction (heart attack) is significantly elevated during the hour after smoking marijuana, even in younger users in their 20s or 30s. Disruption of the normal menstrual cycle can occur. It remains to be determined if male fertility can be affected. CB 2 receptor activation can suppress the immune system, but it has still to be determined if human resistance to infection is altered by marijuana.

Textbook Reference: Cannabis Abuse and the Effects of Chronic Cannabis Exposure 58. In animal studies, what types of brain changes have been observed following adolescent exposure to marijuana?

Answer: Repeated exposure of rodents to cannabinoids during adolescence results in numerous changes in the glutamatergic, GABAergic, and dopaminergic systems. These neurochemical changes are accompanied by altered synaptic plasticity (i.e., LTP and LTD), dysregulated emotional (i.e., anxiety-like and depressive-like) and social behaviors, and impaired cognitive function. Structural studies of the PFC, hippocampus, and nucleus accumbens found evidence for cannabinoid -induced developmental abnormalities of dendritic arbors and spines, with a significant reduction in dendritic length.

Textbook Reference: Cannabis Abuse and the Effects of Chronic Cannabis Exposure

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Test Bank to accompany

Psychopharmacology, Third Edition Meyer • Quenzer

Chapter 15: Hallucinogens, PCP, and Ketamine Multiple Choice 1. Which of the following is not a hallucinogenic drug? a. Mescaline b. LSD c. 5-HT d. DMT Answer: c Textbook Reference: Hallucinogenic Drugs: Introduction 2. Which of the following is not a characteristic that all hallucinogenic drugs have in common? a. They are sometimes taken for spiritual and mystical experiences. b. They can cause cognitive distortions. c. They produce novel perceptual experiences. d. They produce a state of delirium.

Answer: d Textbook Reference: Hallucinogenic Drugs: Introduction 3. Mescaline a. is an alkaloid obtained from various species of mushrooms. b. has been used for years by Native Americans for religious and healing rituals. c. is one of the more popular and readily available hallucinogenic drugs. d. is a synthetic hallucinogen derived from ergot, a fungus that can infest grain.

Answer: b Textbook Reference: Mescaline 4. Which statement about hallucinogenic mushrooms is false? a. They produce mescaline. b. They were used by the Mayan and Aztec civilizations in religious rituals. c. They gave Timothy Leary a start on his journey toward self-discovery with hallucinogenic drugs. d. They were often consumed in ceremonies led by shamans.

Answer: a Textbook Reference: Psilocybin 5. The Harvard Psychedelic Drug Research Program a. was a program that studied the effects of hallucinogenic drugs on animals.

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b. was a complete failure due to the complete lack of control in the studies, causing Leary and Alpert to shut down the program and pursue other research. c. was designed to help people self-administer hallucinogenic drugs in order to free their psyches. d. eventually closed when Leary and Alpert were fired from their jobs as heads of the program, marking an end to the psychedelic movement.

Answer: c Textbook Reference: Psilocybin 6. Ayahuasca a. is a snuff made from South American plants that contains ergot. b. is a preparation that contains AMT and 5-MeO-DMT. c. means ―food for the gods‖ and comes from the peyote cactus. d. is a drink that contains DMT and -carbolines.

Answer: d Textbook Reference: Dimethyltryptamine and Related Tryptamines 7. Hofmann and the Sandoz pharmaceutical company were initially studying LSD-25 because they a. were interested in developing new analeptic drugs. b. wanted to understand the cause of ergotism. c. were trying to prevent premature labor in pregnant women. d. were interested in the role of various compounds in schizophrenia.

Answer: a Textbook Reference: LSD 8. Hoffman’s first LSD exposures a. were universally positive experiences. b. can be characterized as intense perceptual experiences. c. had residual effects that lasted for several days after the drug wore off. d. did not include hallucinations because the dose was so small.

Answer: b Textbook Reference: LSD 9. Researchers have considered LSD as a possible tool for all of the following research approaches or treatment programs except a. as a model for schizophrenia. b. psycholytic therapy. c. psychedelic therapy. d. treatment of anxiety and mood disorders.

Answer: d Textbook Reference: LSD 10. MK-ULTRA was a a. top secret program to control drug use and traffic. b. CIA program designed to evaluate LSD as a mind control agent.

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c. CIA program to record the drug-taking habits of world leaders. d. CIA program to control the drug development agencies.

Answer: b Textbook Reference: LSD 11. What can be said about the status of hallucinogenic drugs today? a. They remain as popular today as they were in the 1960s. b. They were banned in 1967 and as a result have almost completely disappeared today. c. There has been a renewal of interest in these drugs, in part due to clinical research that has been sponsored by the organization MAPS. d. Many psychiatrists and psychologists are now interested in utilizing these drugs in their practices due to a positive shift in government attitudes and policies.

Answer: c Textbook Reference: LSD 12. The most common route of administration for LSD is a. smoking. b. injection. c. topical. d. oral.

Answer: d Textbook Reference: LSD 13. Like , Salvia was historically used in religious rituals by Mazatec shamans. a. mescaline b. LSD c. psilocybin d. DMT Answer: c Textbook Reference: Salvinorin A 14. Salvia differs from other psychedelic drugs in that a. its active ingredient is inactivated in the gastrointestinal tract. b. it produces vivid hallucinations. c. it alters perceptual processes. d. it is entirely legal.

Answer: a Textbook Reference: Salvinorin A 15. The psychedelic with the shortest duration of action is a. LSD. b. psilocybin. c. mescaline. d. DMT. Answer: d Textbook Reference: Pharmacology of Halluncinogenic Drugs

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16. The least potent psychedelic is a. DMT. b. salvinorin A. c. mescaline. d. LSD. Answer: c Textbook Reference: Pharmacology of Halluncinogenic Drugs 17. What experiences characterize the onset of the LSD ―trip‖? a. Feelings of depersonalization b. Synesthesia c. Sensations of colors and geometric shapes d. Suspension of time sense Answer: c Textbook Reference: Pharmacology of Halluncinogenic Drugs 18. Which event does not occur during the plateau or peak of the LSD ―trip‖? a. Experiences of bizarre and sometimes frightening images b. Crossing-over of sensations c. Intensification of the sense of touch d. Time sense distortion Answer: c Textbook Reference: Pharmacology of Halluncinogenic Drugs 19. Why is it not possible to predict whether a user of hallucinogens will have a ―good trip‖ or a ―bad trip‖? a. The drug effects depend very much on the user’s expectations and past experiences with hallucinogens. b. The hallucinogens as a class are very unpredictable and unstable molecules in their effects on the human nervous system. c. The hallucinogens have received virtually no clinical study in humans due to the heavy government restrictions on their use. d. The physiological side effects of the hallucinogens are so dramatic that they make the ―good‖ and ―bad‖ effects difficult to sort out.

Answer: a Textbook Reference: Pharmacology of Halluncinogenic Drugs 20. Most hallucinogens resemble either or in their chemical structure. a. phenethylamines; indoleamines b. indoleamines; carbolines c. carbolines; phenethylamines d. phenethylamines; acetylcholine Answer: a Textbook Reference: Pharmacology of Halluncinogenic Drugs

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21. Which hallucinogenic drug primarily affects norepinephrine at the synapse? a. LSD b. Psilocybin c. Mescaline d. Salvinorin A Answer: c Textbook Reference: Pharmacology of Halluncinogenic Drugs 22. Research on the synaptic effects of LSD and psilocybin has shown all of the following except a. that it binds with high affinity to eight different receptor subtypes. b. that the 5-HT2A receptor appears to play a crucial role in drug-induced hallucinations. c. that D2 dopamine receptors are responsible for the behavioral effects of LSD in animal models. d. that the intensity of psilocybin’s subjective effects is positively correlated with 5-HT2A receptor occupancy.

Answer: c Textbook Reference: Pharmacology of Halluncinogenic Drugs 23. Unlike other hallucinogens, salvinorin A is a. a μ-opioid receptor agonist. b. a κ-opioid receptor agonist. c. a κ-opioid receptor antagonist. d. a μ-opioid receptor agonist and a κ-opioid receptor antagonist.

Answer: b Textbook Reference: Pharmacology of Halluncinogenic Drugs 24. EEG studies have indicated that hallucinogenic drugs can cause an alteration in rhythmic oscillations in pyramidal cells located in the a. cerebral cortex. b. cerebellum. c. amygdala. d. locus coeruleus.

Answer: a Textbook Reference: Pharmacology of Halluncinogenic Drugs 25. Hallucinogenic drugs are not considered to be addictive in the ―classic sense‖ of the word because a. people who use these drugs generally do not experience craving, dependence, or withdrawal. b. users rarely experience adverse effects from the drug experience. c. people simply don’t take these drugs often enough to get addicted to them. d. the high potency and danger of the drugs cause people to take them more cautiously, preventing habitual use.

Answer: a Textbook Reference: Pharmacology of Halluncinogenic Drugs

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26. Which statement about flashbacks is false? a. Scientists do not yet understand the neural mechanism responsible for them. b. They very commonly develop into a more serious and chronic condition called HPPD. c. They occasionally occur following marijuana use. d. They can appear a long time after the drug use during which the hallucinations first occurred.

Answer: b Textbook Reference: Pharmacology of Halluncinogenic Drugs 27. What is the most severe adverse reaction to LSD? a. Flashbacks b. Elevated heart rate c. Frightening hallucinations d. A psychotic breakdown Answer: d Textbook Reference: Pharmacology of Halluncinogenic Drugs 28. Which statement regarding the drug PCP, or phencyclidine, is false? a. It was first tested by a pharmaceutical company as a possible anesthetic agent. b. It causes a trance-like state in which the subject is highly responsive to pain. c. It has a high therapeutic index as it does not cause respiratory depression. d. It is not clinically useful because of side effects of agitation, hallucinations, and violence.

Answer: b Textbook Reference: PCP and Ketamine: Background and History 29. Why did Parke Davis and Company develop ketamine in addition to PCP? a. PCP did not work as effectively as an anesthetic as the researchers had hoped. b. Researchers discovered that PCP caused hallucinations whereas ketamine never caused these adverse reactions. c. The drug company developed ketamine for use in humans and reserved PCP for use in veterinary practice. d. Ketamine was similar to PCP but safer, less potent and shorter-acting.

Answer: d Textbook Reference: PCP and Ketamine: Background and History 30. Which of the following is not a way that PCP or ketamine is typically administered? a. Orally b. Transdermally c. By inhalation or smoking d. Intramuscularly Answer: b Textbook Reference: Pharmacology of PCP and Ketamine

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31. All of the following are subjective experiences reported by individuals after taking low doses of PCP except a. apathy and loneliness. b. expansion of abstract thinking. c. sensations of vertigo or floating. d. cognitive disorganization.

Answer: b Textbook Reference: Pharmacology of PCP and Ketamine 32. At moderate PCP or ketamine doses, individuals experience which phenomena? a. Flashbacks b. Dissociative anesthesia c. HPPD d. Synesthesia Answer: b Textbook Reference: Pharmacology of PCP and Ketamine 33. Which of the following would you expect to observe in an individual experiencing a state of dissociated anesthesia? a. Loss of muscle tone b. Closed eyes c. Detachment from environment d. Relaxed unconsciousness Answer: c Textbook Reference: Pharmacology of PCP and Ketamine 34. When individuals are in the ketamine-induced dissociated state, they report all of the following except a. feeling ―at one‖ with the universe. b. the sense that time is moving at high speed. c. ―near-death‖ experiences. d. visions of spiritual or supernatural beings.

Answer: b Textbook Reference: Pharmacology of PCP and Ketamine 35. PCP and ketamine act on the postsynaptic cell by a. blocking the NMDA receptor at the glutamate site. b. stimulating the receptor where NMDA normally binds. c. acting as a competitive antagonist at the NMDA receptor. d. acting as a noncompetitive antagonists at the NMDA receptor complex.

Answer: d Textbook Reference: Pharmacology of PCP and Ketamine 36. Many of deficits produced by PCP and ketamine can be explained by the action of these drugs on receptors located in the a. basal ganglia and substantia nigra.

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b. cerebral cortex and hippocampus. c. amygdala and hypothalamus. d. pons and midbrain.

Answer: b Textbook Reference: Pharmacology of PCP and Ketamine 37. Self-administration studies in animals have shown that a. both PCP and ketamine are highly reinforcing for several species. b. PCP and ketamine are only moderately rewarding for the species tested. c. the reward effects of PCP and ketamine are unique and not dependent upon dopamine. d. PCP’s reward effects are dopamine-dependent, but ketamine’s effects are dopamineindependent.

Answer: a Textbook Reference: Pharmacology of PCP and Ketamine 38. Which statement about the use and abuse of ketamine is false? a. Ketamine’s popularity can be explained by the fact that the drug does not cause dependence. b. Many abusers of ketamine are medical or veterinary practitioners. c. A number of intellectuals experimented with ketamine as a mind-expanding drug, similar to LSD. d. Ketamine’s use is difficult to track, but is increasing at popular events such as raves.

Answer: a Textbook Reference: Pharmacology of PCP and Ketamine 39. Research has shown that human subjects receiving high doses of ketamine develop symptoms of a. anxiety. b. depression. c. schizophrenia. d. Parkinson’s disease.

Answer: c Textbook Reference: Pharmacology of PCP and Ketamine 40. Studies involving chronic PCP or ketamine administration to nonhuman primates and rodents have demonstrated all of the following neurobiological changes except a. increased NMDA receptor binding in the prefrontal cortex. b. a reduction in tyrosine hydroxylase activity in the prefrontal cortex. c. apoptotic cell death in the developing brain. d. a reduction in glutamatergic synapses in the prefrontal cortex.

Answer: a Textbook Reference: Pharmacology of PCP and Ketamine 41. Which statement about dextromethorphan is false? a. It is an antitussive agent. b. It is a noncompetitive NMDA receptor antagonist.

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c. It is abused on the street as ―Robo‖ or ―DM.‖ d. It affects opiate receptors directly, like codeine.

Answer: d Textbook Reference: Pharmacology of PCP and Ketamine 42. Which statement about dextromethorphan abuse is false? a. It generally involves consuming large amounts of cough syrup or many cold tablets. b. It has generated street sources of dextromethorphan that are repackaged as pills or powder for smoking. c. It often occurs in adolescents and younger children. d. While potentially troubling, it can’t really be dangerous since the drug is available over the counter.

Answer: d Textbook Reference: Pharmacology of PCP and Ketamine

Short Answer/Essay 43. Identify three common characteristics of hallucinogenic drugs. Name two hallucinogenic drugs that have come from nature, and describe the importance of each drug in the history of a people or culture.

Answer: Hallucinogens can produce perceptual and cognitive distortions without producing toxic delirium. Mescaline, from cactus plants, has been used in Mexico for religious and healing rituals. Psilocybin, from mushrooms, has been used in Mexico and Central America, also for religious ceremonies.

Textbook Reference: Hallucinogenic Drugs: Introduction 44. Describe the discovery of LSD by Hoffman and its subsequent applications in research, therapy, and government projects. Where does LSD stand today as a clinical tool?

Answer: Albert Hofmann was making ergot-related derivatives when he noticed unusual feelings and mental state. He wondered if this could have been due to somehow getting the compound he was working on (LSD) into his body. He took a relatively small dose by oral administration (250 micrograms), which we now know is a very large dose, since LSD is extremely potent. He experienced a very large effect, including visual distortions and a feeling of being outside of his body. Since the structure of LSD resembles serotonin, one of our natural neurotransmitters, this discovery fostered a great deal of research into possible biochemical causes of hallucinations, such as can occur in schizophrenia. The U.S. Army carried out experiments with LSD to see if it could be used as a weapon or a mind control agent. Agents such as LSD, psilocybin, and ecstasy are being examined in trial studies to see if they can aid in the treatment of post-traumatic stress disorder (PTSD) or depression associated with terminal illnesses.

Textbook Reference: LSD 45. Describe the typical stages of an LSD ―trip,‖ including onset and duration. How is DMT different from LSD in terms of time course of action?

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Answer: The LSD trip can be divided into four phases: onset, plateau, peak, and ―comedown.‖ Trip onset occurs about 30 minutes to an hour after one takes LSD. Visual effects begin to occur, with intensification of colors and the appearance of geometric patterns or strange objects that can be seen with one’s eyes closed. The next 2 hours of the trip represent the plateau phase. The subjective sense of time begins to slow and the visual effects become more intense during this period. The peak phase generally begins after about 3 hours and lasts for another 2–3 hours. During this phase, users might feel as if they are in another world in which time has been suspended. Users may see a continuous stream of bizarre, distorted images that may be either beautiful or menacing.

Users may experience synesthesia, a crossing-over of sensations in which, for example, colors are ―heard‖ and sounds are ―felt.‖ The peak is followed by the comedown, a phase lasting 2 hours or longer, depending on the dose. Most of the drug effects are gone by the end of the comedown, although the user may still not feel completely normal until the following day. In addition to the sensory–perceptual effects just described, hallucinogenic drugs can also produce feelings of depersonalization, emotional shifts to a euphoric or to an anxious and fearful state, and disruption of logical thought. Because DMT is metabolized so quickly, its duration of action is much shorter compared to LSD. A DMT experience may only last 30–60 minutes. When combined with a monoamine oxidase (MAO) inhibitor, however, as in ayahuasca, the DMT experience will last much longer.

Textbook Reference: LSD 46. Explain the difference between indoleamine and phenethylamine hallucinogens. Give an example of each. What receptors do these hallucinogens act on? How does salvinorin A fit into the hallucinogen family?

Answer: Phenethylamine compounds, such as mescaline, have a structural resemblance to catecholamines, while indoleamine compounds, such as LSD, have a structural resemblance to serotonin. Serotonin receptor activation appears to be necessary for hallucinogenic activity, especially the 5-HT2A receptor. Salvinorin A appears to differ with regard to receptor activation, in this case instead of activating 5-HT2A receptors, salvinorin A action may require activation of the κ-opiate receptor.

Textbook Reference: Pharmacology of Halluncinogenic Drugs 47. Describe the following possible adverse reactions to hallucinogenic drug use: a ―bad trip,‖ flashbacks, and HPPD. What is the most severe adverse reaction to LSD use?

Answer: The user may have a ―bad trip‖ in which she experiences an acute anxiety or panic reaction in response to the drug’s effects. Flashbacks are transient re-experiences of some of the visual distortions that occurred during previous episodes of hallucinogen usage. Users typically do not consider occasional flashbacks to be distressing, and some users even refer to them as ―free trips.‖ Hallucinogen persisting perception disorder (HPPD) is a more serious disturbance in which severe perceptual symptoms persist for a long period of time following drug use and are experienced sufficiently frequently to cause significant distress or impairment to the individual.

Textbook Reference: Pharmacology of Halluncinogenic Drugs 48. Distinguish between PCP and ketamine in terms of their pharmaceutical development, safety, and effects. Are these drugs used recreationally?

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Answer: PCP was developed in the 1950s for use as an anesthetic. It produces a detached (dissociated) state and has less risk of respiratory depression compared to other anesthetics, but it can also produce agitation and post-operative effects such as hallucinations. The structurally related ketamine was developed as a less potent, shorter acting compound compared to PCP. It can produce some of the same side effects as PCP, but less so in children, and it is used in veterinary medicine as an anesthetic. Both of these drugs have been used for recreational purposes.

Textbook Reference: Pharmacology of PCP and Ketamine 49. Describe the subjective and behavioral effects of low-dose PCP. What happens when subjects are given higher doses? List several experiences reported by ketamine users while in the dissociated state (some associated with the K-hole).

Answer: When given a subanesthetic dose of PCP, subjects report feeling detached from their bodies, sensations of vertigo or of floating, numbness, and sometimes a dreamlike state. They also experienced a variety of affective reactions including drowsiness and apathy, loneliness, negativism or hostility toward the experimenters, or, alternatively, feelings of euphoria and inebriation. At higher doses, individuals exhibited a marked cognitive disorganization manifested by difficulty in maintaining concentration or focus, deficiencies in abstract thinking, and halting speech. With ketamine, the individual may feel separated from his body, perhaps floating above and looking down at himself. Some have described this as a ―near-death‖ experience even though the person is not actually dying. This state of being, which is called the ―K-hole,‖ can be either spiritually uplifting or terrifying.

Textbook Reference: Pharmacology of PCP and Ketamine 50. Using data from animal studies and reports from human users, determine the reward value of PCP and ketamine. In other words, how much do people and animals like thesedrugs, and how do we know?

Answer: Rats and primates will self-administer PCP and ketamine. Primate studies indicated that the animals would produce a very high state of intoxication. These drugs can stimulate firing of the pathway from the ventral tegmentum to the nucleus accumbens, suggesting the importance of dopamine release in the accumbens, although PCP will be self-administered even if put directly in the accumbens, which may not involve dopamine release. Human studies have also indicated a positive feeling (drug ―liking‖) for these agents, as monitored by subjective rating response s.

Textbook Reference: Pharmacology of PCP and Ketamine 51. Where do PCP and ketamine exert their effects at the synapse? Be specific. How might this relate to some of the cognitive changes that occur in the drug state?

Answer: Both drugs are noncompetitive inhibitors of the glutamate NMDA receptor.

NMDA receptors have been shown to play a prominent role in the production of longterm potentiation, a model for alterations in synaptic plasticity that may relate to learning and memory. In some brain areas (e.g., anterior cingular cortex), this inhibition of NMDA receptors may produce an increase in glutamate release.

Textbook Reference: Pharmacology of PCP and Ketamine

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52. What makes certain types of cough syrup and cold tablets attractive to individuals looking for a PCP-like drug experience? Identify the active ingredient in this process, and explain how it works in the nervous system.

Answer: Dextromethorphan is in cough syrup to suppress coughing. It is metabolized to dextrorphan. Along with other pharmacological properties, these two agents can noncompetitively inhibit the NMDA receptor, which is an action they share with PCP and ketamine. It is this property that could lead to recreational use of cough syrup to mimic the behavioral effects of PCP and ketamine. At doses of dextromethorphan ranging from 300 to 600 mg, the user may experience intense hallucinations, cognitive impairment, and partial dissociation. At doses of more than 600 mg of dextromethorphan, the user becomes severely ataxic, experiences complete personality dissociation, and may become delusional. These effects resemble those produced by increasing doses of PCP or ketamine.

Textbook Reference: Pharmacology of PCP and Ketamine

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Test Bank to accompany

Psychopharmacology, Third Edition Meyer • Quenzer

Chapter 16: Inhalants, GHB, and Anabolic–Androgenic Steroids Multiple Choice 1. Inhalants a. are substances such as glues and contact cement that can cause a temporary ―high‖ but are rarely dangerous. b. include illegal abused substances such as Resistol. c. have been linked to long-term damage to the brain and other organs. d. are mainly abused in other countries; children in the United States have generally not used or abused these drugs.

Answer: c Textbook Reference: Inhalants: Introduction 2. Which of the following is not a characteristic of abused inhalant drugs? a. They must be volatile liquids or gases. b. They are relative newcomers to the drug abuse scene. c. The route of administration involves sniffing, inhaling, or spraying an aerosol. d. While humans find inhalant drugs to be reinforcing, animals do not.

Answer: d Textbook Reference: Inhalants: Background 3. With regard to types of inhalants, a. sources of aerosols include propane tanks, refrigerants, and butane lighters. b. volatile solvents include adhesives, ink, and correction fluid. c. nitrites such as ―poppers‖ act directly on the brain to increase sexual arousal. d. gases include hair sprays, deodorant sprays, and spray paints.

Answer: b Textbook Reference: Inhalants: Background 4. Regarding patterns and demographics of inhalant use, a. surveys indicate that inhalants are the most popular abused substances of 12-year-olds. b. government studies show that 15% of children have tried inhalants by the fourth grade. c. initial inhalant use almost always follows experimentation with alcohol or tobacco. d. among children in middle school, inhalants are second to marijuana in popularity.

Answer: a Textbook Reference: Inhalants: Background

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5. The immediate effects of volatile and gaseous inhalants are similar to those seen following use of a. opiates. b. cannabinoids. c. alcohol. d. indoleamine hallucinogens.

Answer: c Textbook Reference: Inhalants: Behavioral and Neural Effects 6. All of the following symptoms have been observed during the abuse of inhalants except a. euphoria. b. hallucinations. c. delusions. d. mania.

Answer: d Textbook Reference: Inhalants: Behavioral and Neural Effects 7. Which statement does not support the idea that inhalants are addictive substances? a. Inhalants cause a period of disinhibition or stimulation, followed by drowsiness. b. Animals show a significant preference for the compartment in which they had been exposed to the inhalant toluene. c. There is some evidence that there is a withdrawal syndrome from inhalants characterized by tremors, irritability, and sleep problems. d. People repeatedly use inhalants in spite of the risk of brain injury, damage to other organs, and death.

Answer: a Textbook Reference: Inhalants: Behavioral and Neural Effects 8. Why is it particularly difficult to study the mechanism of action of inhalants? a. Scientists do not understand their absorption and distribution in the body. b. There is tremendous chemical diversity in this group of drugs, and it is likely that they may work in different ways. c. These substances have arrived recently on the drug abuse scene and most researchers have not considered their dangers serious enough to merit study. d. It is very difficult to design inhalant studies in animals, and the number of human users is too small to generate significant data.

Answer: b Textbook Reference: Inhalants: Behavioral and Neural Effects 9. Studies have shown that radiolabeled toluene injected into the brain disproportionately labels the a. frontal cortex and cerebellum. b. hippocampus and thalamus. c. striatum and cerebellum. d. frontal cortex and hippocampus.

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Answer: c Textbook Reference: Inhalants: Behavioral and Neural Effects 10. Which of the following is not an effect of inhalants on the CNS? a. They enhance the function of GABA A receptors. b. They block NMDA glutamate receptors. c. They activate DA in the VTA. d. They inhibit the activity of glycine receptors.

Answer: d Textbook Reference: Inhalants: Behavioral and Neural Effects 11. Inhalants inhibit the CNS and impair behavior in a manner similar to a. the cannabinoids. b. alcohol. c. the opioids. d. GHB. Answer: b Textbook Reference: Inhalants: Behavioral and Neural Effects 12. Many inhalants enhance the activity of receptors and inhibit the activity of receptors. a. GABA A; NMDA b. NMDA; GABA A c. nicotinic; NMDA d. GABA A; dopamine Answer: a Textbook Reference: Inhalants: Behavioral and Neural Effects 13. While not common, a single use of inhalants can potentially be fatal, an effect known as a. myocardial infarction. b. sudden inhalant death syndrome. c. sudden sniffing death syndrome. d. inhalant toxicity syndrome.

Answer: c Textbook Reference: Inhalants: Behavioral and Neural Effects 14. All of the following are health risks of inhalant use except a. fatal cardiac arrhythmia. b. coronary heart disease. c. damage to myelin sheaths surrounding axons. d. subcortical abnormalities in the cerebellum, pons, and basal ganglia.

Answer: b Textbook Reference: Inhalants: Behavioral and Neural Effects 15. It is thought that GHB may be co-released with GABA upon neuronal firing because

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a. it can be taken up into GABAergic vesicles. b. it is produced during the synthesis of GABA. c. GABA is metabolized into GHB in the vesicles. d. GHB easily passes through vesicular membranes.

Answer: a Textbook Reference: Gamma-Hydroxybutyrate: Background 16. Which statement regarding GHB or γ-hydroxybutyrate is false? a. It is structurally similar to GABA. b. It was first studied by Laborit who was seeking a CNS depressant for therapeutic applications. c. It produces sedation and anesthesia in animals and humans. d. It is available over-the-counter for use as a sedative.

Answer: d Textbook Reference: Gamma-Hydroxybutyrate: Background 17. Which of the following is not a reason that GHB became controversial in the United States? a. The FDA received reports of illnesses related to GHB, and subsequently banned overthe-counter sales. b. Health food stores marketed GHB as an easy way to lose weight and enhance athletic endurance. c. It enjoyed popularity as a recreational drug at nightclubs and raves, especially among teens. d. It was synthesized from ―home kits,‖ circumventing attempts to control access to the drug.

Answer: b Textbook Reference: Gamma-Hydroxybutyrate: Background 18. Which statement about ―date rape‖ drugs is false? a. They cause amnesia for the rape, which limits the ability to prosecute the rapist. b. The government recently passed legislation to increase the penalties for sale or possession of these drugs. c. The Drink Safe Coaster is a reliable way to test drinks for the presence of Rohypnol and GHB. d. The pharmaceutical company has reformulated Rohypnol so that it turns blue when dissolved in alcohol to discourage its use as a ―rape drug.‖ Answer: c Textbook Reference: Gamma-Hydroxybutyrate: Background 19. Low doses of GHB produce all of the following except a. disinhibition. b. mild euphoria. c. calmness and relaxation. d. perceptual disturbances.

Answer: d

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Textbook Reference: Gamma-Hydroxybutyrate: Behavioral and Neural Effects 20. Which of the following is not a symptom experienced following high doses of GHB? a. Rapid respirations b. Vomiting c. Dizziness d. Ataxia Answer: a Textbook Reference: Gamma-Hydroxybutyrate: Behavioral and Neural Effects 21. GHB has all of the following effects in animals except a. increased anxiety in the elevated plus maze. b. hypolocomotion. c. sedation. d. catalepsy.

Answer: a Textbook Reference: Gamma-Hydroxybutyrate: Behavioral and Neural Effects 22. Animal studies designed to measure the reward value of GHB a. have been consistent with human studies. b. have shown positive findings in self-administration paradigms but not placeconditioning tasks. c. have found even stronger evidence for the reinforcing effects of GHB than in human studies. d. are inconsistent, with rodents showing positive findings and monkeys demonstrating variable results.

Answer: d Textbook Reference: Gamma-Hydroxybutyrate: Behavioral and Neural Effects 23. Some researchers believe that GHB’s effects are mediated by a specific receptor.

Which statement about this proposed receptor is not accurate? a. The receptor belongs to the superfamily of G protein–coupled metabotropic receptors. b. The receptor’s gene has not been cloned; therefore, the structure of the receptor is unknown. c. The presence of a GHB receptor suggests the existence of endogenous GHB, which is in fact synthesized from GABA. d. The highest level of binding for the receptor is in the cerebellum and brain stem.

Answer: b Textbook Reference: Gamma-Hydroxybutyrate: Behavioral and Neural Effects 24. Which statement supports the hypothesis that GHB acts on the GABA B receptor? a. GHB has definitively been shown to be metabolized in the brain to GABA, which then stimulates GABA B receptors. b. GHB has been shown to have a high affinity for the GABA B receptor. c. The behavioral and physiological effects of GHB can be reversed by baclofen.

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d. Mice genetically engineered to lack the GABA B receptor do not show behavioral or physiological responses to GHB. Answer: b Textbook Reference: Gamma-Hydroxybutyrate: Behavioral and Neural Effects 25. GHB’s only legitimate use in the United States is a. as an anesthetic. b. as a sleep aid. c. to treat anxiety. d. to treat narcolepsy.

Answer: d Textbook Reference: Medical and Recreational Uses for GHB 26. With respect to GHB tolerance, dependence, and withdrawal, a. tolerance to GHB has been found in animal studies. b. anecdotal reports suggest that dependence does not develop with repeated use of GHB. c. withdrawal symptoms are mild (sleep disruption), even at very high doses. d. tolerance to GHB in humans has been well-studied and does not seem to exist.

Answer: a Textbook Reference: Medical and Recreational Uses for GHB 27. Which statement about anabolic–androgenic steroids is false? a. They increase muscle mass. b. They are always injected intramuscularly. c. They have masculinizing properties. d. They are used and abused as performance enhancers.

Answer: b Textbook Reference: Anabolic–Androgenic Steroids: Background and History 28. The core structure of anabolic steroids is formed by a. oxandrolone. b. nandrolone. c. stanozolol. d. testosterone.

Answer: d Textbook Reference: Anabolic–Androgenic Steroids: Background and History 29. According to the history of anabolic steroid use, a. the East Germans were the first to use these drugs as performance enhancers in weightlifting competition. b. the United States did not administer these drugs to its elite athletes until the late 1980s. c. Oral-Turabinol use by female athletes in the GDR was linked to many achievements and Olympic medals. d. although these drugs have been abused by many professional athletes, very few college and high school athletes have access to them.

Answer: c

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Textbook Reference: Anabolic–Androgenic Steroids: Background and History 30. Which of the following is not a reason that people who take anabolic steroids might engage in a pattern of use called cycling? a. To allow time for the use of a second steroid b. To avoid unpleasant side effects c. To minimize the development of tolerance d. To avoid detection of a banned substance Answer: a Textbook Reference: Anabolic–Androgenic Steroids: Background and History 31. What pattern of steroid use might an endurance athlete or a sprinter choose? a. Stacking b. High doses right before the event c. Pyramiding d. Low doses Answer: d Textbook Reference: Anabolic–Androgenic Steroids: Background and History 32. Controlled studies of the effects of anabolic steroids on muscle strength, muscle size, and sexual function showed all of the following except a. a dose-dependent increased in size of the quadriceps muscle. b. an increase in leg press strength. c. a dose-dependent increase in thigh muscle volume. d. a large increase in sexual drive or activity.

Answer: d Textbook Reference: Pharmacology of Anabolic–Androgenic Steroids 33. Which statement regarding androgen receptors is false? a. They are found in muscle tissue, where they increase protein synthesis and muscle growth when activated by androgens. b. They are found in the cytoplasm of the cell. c. They translocate into the cell nucleus when bound to an androgen. d. When activated, they shut down gene transcription.

Answer: d Textbook Reference: Pharmacology of Anabolic–Androgenic Steroids 34. Recent studies indicate that anabolic steroids promote the and increase the production of . a. differentiation of stem cells into muscle cells; cells that can become muscle fibers b. synthesis of androgen receptors; testosterone c. production of smooth muscle; testosterone d. insertion of androgen receptors into the membrane; transcription factors sensitive to androgens Answer: a Textbook Reference: Pharmacology of Anabolic–Androgenic Steroids

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35. Which statement concerning the side effects of anabolic steroids is true? a. The masculinizing effects of steroids on women are reversible side effects. b. The idea that steroids ―stunt your growth‖ is merely a popular myth. c. Common effects of steroid use include acne and cardiovascular problems. d. Studies show that ―roid rage‖ is a very common response to anabolic steroid use.

Answer: c Textbook Reference: Pharmacology of Anabolic–Androgenic Steroids 36. Specific effects of anabolic steroids on males and females include all of the following except a. smaller testes in males. b. shrinking of the prostate in males. c. breast development in males. d. enlarged clitoris in females.

Answer: b Textbook Reference: Pharmacology of Anabolic–Androgenic Steroids 37. In addition to their desired effects on muscle, anabolic steroids negatively affect several physiological systems, including the heart, , and . a. kidneys; gastrointestinal system b. immune system; liver c. kidneys; liver d. immune system; gastrointestinal system Answer: c Textbook Reference: Pharmacology of Anabolic–Androgenic Steroids 38. According to the story of Mr. X and other case studies, which statement regarding ―roid rage‖ is false? a. It can involve extreme violence, even murder. b. It doesn’t occur unless there is a history of psychiatric illness. c. It can occur for short periods of time in otherwise quiet and considerate people. d. It seems to occur in a particularly susceptible subset of individuals.

Answer: b Textbook Reference: Pharmacology of Anabolic–Androgenic Steroids 39. Heavy users of anabolic steroids may show all of the following psychological or behavioral symptoms except a. a perception that the user is weak and small. b. increased irritability or anxiety. c. impaired cognitive function. d. depressed mood during withdrawal.

Answer: c Textbook Reference: Pharmacology of Anabolic–Androgenic Steroids 40. Dependence on anabolic steroids is

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a. supported by many studies in the literature suggesting users meet most of the DSM criteria for substance abuse and withdrawal. b. supported by the fact that many individuals are seeking help for problems stemming from anabolic steroid abuse. c. shown in the strong cravings reported by users who are no longer taking steroid drugs. d. shown in the report that even first-time steroid users find the drugs to be rewarding and desirable.

Answer: a Textbook Reference: Pharmacology of Anabolic–Androgenic Steroids 41. The reinforcing properties of anabolic steroids a. are demonstrated in self-administration and place conditioning studies in animals. b. are produced by activation of intracellular androgen receptors. c. can be seen immediately in human users as euphoria. d. are amplified in rats genetically engineered to have nonfunctional androgen receptors.

Answer: a Textbook Reference: Pharmacology of Anabolic–Androgenic Steroids

Short Answer/Essay 42. Identify the four different types of inhalants that are abused, and give a few examples from each category. What three characteristics do all inhalants have in common?

Answer: The four types are volatile solvents (examples: toluene, xylene, acetone); fuels (examples: butane, propane); halogenated hydrocarbons (examples: trichloromethane, trichoroethane); and anesthetics (examples: chloroform, ether, nitrous oxide). All inhalants are volatile or gaseous at room temperature, taken in by inhaling fumes or spraying into nose or mouth, and do not belong to the class of agents that are taken into the lungs by smoking, such as nicotine or THC. Textbook Reference: Inhalants: Background 43. Describe the ways in which the inhalants are similar to alcohol. Include information about their acute and chronic effects, mechanism of action, and impact on fetal development.

Answer: Like alcohol, inhalants can produce euphoria, stimulation, and disinhibition.

High levels produce ataxia, slurred speech, hallucinations, and poor coordination, similar to alcohol. Chronic use can produce tolerance, and withdrawal symptoms include nausea, fatigue, irritability, anxiety, and sleep disturbances. Increased firing of dopaminergic neurons in the ventral tegmentum may contribute to inhalant dependence. Agents like toluene can enhance GABA A receptor activity and decrease NMDA activity, again similar to ethanol action. Inhalant-using or occupationally-exposed pregnant women are more likely to have premature births, lower weight births, and can produce offspring with symptoms resembling fetal alcohol syndrome, in what has been term fetal solvent syndrome.

Textbook Reference: Inhalants: Behavioral and Neural Effects

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44. What is known about the action of inhalants in the CNS? Are these substances reinforcing in the same manner as other drugs studied in this text? How do you know?

Why are inhalants particularly difficult to study as a class of drugs?

Answer: Inhalants can activate the ventral tegmental dopamine pathway that innervates the nucleus accumbens, a property in common with many reinforcing drugs. Place preference tests with toluene have demonstrated this reinforcing property of inhalants.

Having so many diverse compounds classified as inhalants can make generalizations about their actions problematic.

Textbook Reference: Inhalants: Behavioral and Neural Effects 45. Describe the discovery and early marketing/promotion of GHB by health food stores.

Why is GHB called a ―club drug‖? What problems with the drug led to its being classified as a Schedule I drug in 2000?

Answer: GHB was purported to lower body fat and increase body muscle mass, which would especially appeal to bodybuilders. People at dance clubs report that they use GHB to feel relaxed, euphoric, or sexually aroused. Evidence for reinforcing effects of GHB, both in animals and humans, and its intoxicating and sedative effects, suggested that it should be classified as a Schedule I drug.

Textbook Reference: Gamma-Hydroxybutyrate: Background 46. How is GHB typically consumed? Explain how the effects of GHB have led to its use as a ―date rape drug.‖ Name two other drugs that are also used in this manner. What can be done to protect against this type of threat?

Answer: GHB is typically taken by the oral route of administration. The fact that it can cause sedation and amnesia has made it popular as a ―date rape drug.‖ The amnesia may make legal prosecution for rape more difficult. Other date rape drugs include flunitrazapam (Rohypnol) and alprazolam (Xanax). Not accepting drinks from strangers or leaving your drink unattended are two ways to reduce the risk of unknowingly ingesting a date rape drug.

Textbook Reference: Gamma-Hydroxybutyrate: Background 47. Describe the current knowledge regarding GHB binding sites in the brain. Consider both endogenous and exogenous GHB. Answer: Binding sites for GHB exist in the nucleus accumbens, hippocampus, and cerebral cortex. The finding that GHB can bind to certain subtypes of GABA A receptors can complicate the interpretation of these binding studies. When administered, the high levels of GHB that will be reached in the brain can also bind to GABA B receptors. This can be of importance with regards to behavioral effects of administered GHB, since behavioral effects of GHB in rodents can be antagonized in GABA B mouse knockouts, and by GABA B receptor antagonists.

Textbook Reference: Gamma-Hydroxybutyrate: Behavioral and Neural Effects 48. Describe the therapeutic uses of GHB/sodium oxybate in the United States and Europe. What measures have been taken to prevent recreational use of this compound?

Answer: GHB has been approved in the United States for the treatment of narcolepsy. In Europe, it is approved for use as an intravenous anesthetic and in the treatment of alcohol

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addiction. Measures to prevent misuse of this compound include: single-source manufacture, distribution through a central pharmacy, education of physicians and patients on appropriate use of the medication, and patient and physician registries.

Textbook Reference: Medical and Recreational Uses for GHB 49. Briefly describe the historical use of anabolic steroids in the Soviet Union, United States, and East Germany. What legislation changed this state of affairs in the United States?

Answer: In the 1950s it was revealed that Soviet weight lifters were using testosterone to increase athletic performance. Methandrostenolone (Dianabol) was developed in the United States to have a compound which had more anabolic (muscle building) properties compared to androgenic properties. In the 1960s male and female athletes from East Germany were using anabolic steroids. In the United States, the Anabolic Steroids Control Act was passed by Congress in 1990. Anabolic steroids were classified as Schedule III substances, requiring a medical prescription. In addition, many athletic organizations in the United States banned the use of anabolic steroids.

Textbook Reference: Anabolic–Androgenic Steroids: Background and History 50. List four reasons why a steroid user might engage in the practice of cycling. Describe two other patterns of use that are sometimes combined with cycling.

Answer: Steroid users might engage in cycling to avoid developing tolerance, reduce side effects, maximize athletic performance in competition, or avoid detection of use. Other patterns include pyramiding, in which the dose is gradually increased, and then gradually decreased, and stacking, in which two or more anabolic steroids are taken, sometimes a short-acting steroid combined with a longer-acting steroid.

Textbook Reference: Anabolic–Androgenic Steroids: Background and History 51. Summarize the results of studies by Bhashin and colleagues that investigated the effects of testosterone on muscle size, muscle strength, and sexual function.

Answer: Dose-dependent increases in muscle size and strength were produced, and no change in sexual function (sexual activity, desire).

Textbook Reference: Pharmacology of Anabolic–Androgenic Steroids 52. Explain how anabolic steroids can lead to increased muscle mass. Include steroid action at the testosterone receptor and two additional mechanisms.

Answer: The steroid crosses the plasma membrane and combines with a steroid receptor in the cell. These then travel to the nucleus, where they can influence gene expression that results in an increase in proteins that will increase muscle mass and strength. In addition, satellite cells proliferate and stimulate myotube formation, which helps in the formation of new muscle fibers, and there is also an increase in the conversion of stem cells into muscle cells, as opposed to forming adipose cells.

Textbook Reference: Pharmacology of Anabolic–Androgenic Steroids 53. Identify several side effects of anabolic steroid use. List two effects that are specific to male users and two that are specific to females.

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Answer: General side effects include hypertension, impaired renal function, and acne.

Side effects for males include testicular shrinkage and reduced sperm count; for females, menstrual abnormalities and decreased breast size.

Textbook Reference: Pharmacology of Anabolic–Androgenic Steroids 54. Discuss what the literature and case studies have to say about the likelihood of anabolic steroids causing aggression and ―roid rage.‖ Is the case of Mr. X typical or not?

Answer: Anabolic steroids can cause mood alterations, such as irritability, hypomania, or even mania. In addition, depression may occur during steroid withdrawal. The violence of Mr. X is not considered typical, but is viewed as something that can occur in a subset of anabolic steroid users.

Textbook Reference: Pharmacology of Anabolic–Androgenic Steroids 55. List the ways in which anabolic steroid use meets the criteria for drug dependence. In what ways is steroid use atypical?

Answer: About one-third of chronic anabolic steroid users meet at least three of the criteria established by the American Psychiatric Association for drug dependence. These symptoms include tolerance, withdrawal, taking the substance in larger amounts than intended, inability to cut down or control use of the substance, significant amount of time spent on substance-related activity, other activities reduced in favor of substance use, and continued substance use despite recognition of use-related problems. Differences compared to other drug dependent–producing agents include a lack of euphoric feeling with anabolic steroids, less significant impairment of daily activities, and less likelihood that anabolic steroid users will seek treatment for their drug use.

Textbook Reference: Pharmacology of Anabolic–Androgenic Steroids

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Test Bank to accompany

Psychopharmacology, Third Edition Meyer • Quenzer

Chapter 17: Disorders of Anxiety and Impulsivity and the Drugs Used to Treat These Disorders Multiple Choice 1. Anxiety disorders a. affect about 40% of Americans at some point in their lives. b. are associated with major depression in about 35% of people. c. include episodes of panic, phobic avoidance behaviors, and compulsive rituals. d. are less disabling than other mental illnesses because anxiety has survival value.

Answer: c Textbook Reference: Neurobiology of Anxiety 2. All of the following occur during anxiety except a. stimulation of the parasympathetic nervous system. b. sleep disturbances. c. activation of the fight-or-flight response. d. impaired concentration.

Answer: a Textbook Reference: Neurobiology of Anxiety 3. Acute anxiety can be most effectively treated with a. tricyclic antidepressants. b. cognitive behavior therapy. c. benzodiazepine medications. d. barbiturates.

Answer: c Textbook Reference: Neurobiology of Anxiety 4. What area of the brain coordinates the components of anxiety and other emotions? a. Hypothalamus b. VTA c. Locus coeruleus d. Amygdala Answer: d Textbook Reference: Neurobiology of Anxiety 5. In addition to the central nucleus of the amygdala, the appears to play an important role in initiating sustained emotional responses of anxiety when danger signals are unclear.

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a. hippocampus b. BNST c. lateral nucleus of the amygdala d. prefrontal cortex Answer: b Textbook Reference: Neurobiology of Anxiety 6. What area of the brain exerts inhibitory control over the areas involved in emotions? a. Parietal cortex b. Prefrontal cortex c. Limbic system d. Temporal cortex Answer: b Textbook Reference: Neurobiology of Anxiety 7. Which statement about CRF is false? a. CRF acts as both a hormone and a neurotransmitter. b. Hormonal CRF activates the pituitary glands during stress. c. CRF antagonists that reduce stress or anxiety have not yet been discovered. d. High levels of CRF receptors are found in brain regions involved in anxiety.

Answer: c Textbook Reference: Neurobiology of Anxiety 8. Which statement about the role of norepinephrine in anxiety is false? a. Inhibition of the locus coeruleus can elicit alerting and fear responses in animals. b. Abnormal sympathetic nervous system activation is a common feature of anxiety disorders. c. Excess norepinephrine activity can contribute to the formation of trauma memories in PTSD. d. Some anxiety-reducing drugs work by inhibiting norepinephrine pathways.

Answer: a Textbook Reference: Neurobiology of Anxiety 9. Administration of before retrieval of a traumatic memory seems to diminish the emotional aspects of the memory without affecting the memory itself, suggesting a role for these drugs in the treatment of . a. a CRF antagonist; specific phobia b. a β-blocker; PTSD c. a benzodiazepine; PTSD d. yohimbine; GAD Answer: b Textbook Reference: Neurobiology of Anxiety 10. Which of the following is not an effect of anxiety-reducing drugs on locus coeruleus (LC) cell firing? a. TCAs enhance norepinephrine action at inhibitory autoreceptors to reduce LC firing.

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b. Benzodiazepines increase the inhibitory effects of GABA on the cells in the LC. c. SSRIs increase serotonin, which inhibits LC firing. d. Yohimbine increases serotonin and norepinephrine, resulting in a decrease in LC firing.

Answer: d Textbook Reference: Neurobiology of Anxiety 11. Which statement regarding the role of GABA in anxiety is false? a. The GABA drug muscimol causes anxiety. b. Intracranial injections of benzodiazepines reduce anxiety in operant conflict tasks. c. Bicuculline blocks benzodiazepine-enhancement of behavior in the social interaction test in animals. d. Benzodiazepine injections into the amygdala increase the number of light–dark crossings in animals.

Answer: a Textbook Reference: Neurobiology of Anxiety 12. Neurosteroids exert their effects by _ . a. anxiogenic; increasing LC firing b. anxiolytic; activating the prefrontal cortex c. anxiolytic; enhancing GABA’s effect on chloride channels d. anxiogenic; activating the hippocampus Answer: c Textbook Reference: Neurobiology of Anxiety 13. The research linking serotonin to anxiety is mostly based on a. levels of serotonin turnover and metabolites in anxious individuals. b. the fact that benzodiazepines have major effects of the serotonin system. c. the monoamine hypothesis of anxiety, which is widely accepted. d. the mechanism of action of anxiolytic drugs like BuSpar and the SSRIs. Answer: d Textbook Reference: Neurobiology of Anxiety 14. Dopamine plays a modulatory role in anxiety by apparently inhibiting thus increasing activation of the . a. inhibitory control from the prefrontal cortex; amygdala b. the amygdala; prefrontal cortex c. the hypothalamus; sympathetic nervous system d. VTA; prefrontal cortex Answer: a Textbook Reference: Neurobiology of Anxiety

and

15. Which statement about adult mice exposed to early prenatal stress is false? a. They show enhanced HPA axis activity in response to stress. b. They show disrupted negative feedback of the HPA axis. c. They have increased numbers of glucocorticoid receptors.

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d. They show increased expression of CRF in the amygdala.

Answer: c Textbook Reference: Neurobiology of Anxiety 16. The consequences of early exposure to stress include and . a. atrophy of the amygdala; genetics; gender b. HPA axis response to stress; timing of stressor; gender c. hyperactivity; age; ethnicity d. cognitive changes; nutritional status; history of substance use Answer: b Textbook Reference: Neurobiology of Anxiety

and depend on both

17. Which of the following is not a clinical anxiety disorder recognized by the American Psychiatric Association? a. Panic attacks b. Obsessive–compulsive disorder c. Phobias d. Acute anxiety Answer: d Textbook Reference: Characteristics of Anxiety Disorders 18. Generalized anxiety disorder (GAD) a. is one of the least common anxiety disorders. b. starts in the teens or twenties and persists throughout life. c. will lead to agoraphobia if untreated. d. is genetically determined, as twin studies strongly indicate.

Answer: b Textbook Reference: Characteristics of Anxiety Disorders 19. Which statement about panic disorder is false? a. The individual experiences intense parasympathetic arousal. b. The individual feels like they are going to die or lose control. c. The unpredictable nature of the attacks creates a feeling of anticipatory anxiety. d. The worry of having attacks in unsafe places often leads to the development of agoraphobia.

Answer: a Textbook Reference: Characteristics of Anxiety Disorders 20. Which of the following has not been implicated as a risk factor or triggers in panic disorder? a. Genetic predisposition for panic b. Breathing air with decreased amounts of carbon dioxide c. Injection with lactic acid d. Yohimbine injection Answer: b

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Textbook Reference: Characteristics of Anxiety Disorders 21. During an induced panic attack, an increase in the physiological signs of panic could be caused by , and increased activity of the would make the person more aware of those sensations. a. increased activity of the hippocampus; amygdala b. decreased activity of the prefrontal cortex; sympathetic nervous system c. increased activity of the amygdala; insula d. increased activity of the insula; prefrontal cortex Answer: c Textbook Reference: Characteristics of Anxiety Disorders 22. Which statement about phobias is false? a. They involve fears that the person recognizes as extreme or irrational. b. They are in part determined by culture; for example the Chinese often fear the cold and loss of body heat. c. They are effectively treated by having the person relax while presenting the feared stimulus in gradually increasing intensities. d. They are rarely so severe that they affect the quality of a person’s life.

Answer: d Textbook Reference: Characteristics of Anxiety Disorders 23. Which statement about post-traumatic stress disorder (PTSD) is false? a. It has been diagnosed in very few soldiers returning from the wars in Iraq and Afghanistan. b. It occurs in people who have experienced or witnessed traumatic events, such as the 9/11 terrorist attacks. c. It is characterized by nightmares and flashbacks in which people relive the traumatic event. d. It is associated with increased physiological and psychological reactivity to events that are related to the trauma.

Answer: a Textbook Reference: Characteristics of Anxiety Disorders 24. Which of the following is not a reliable symptom or characteristic of PTSD? a. Sleep disturbances b. Numbing of emotional responses c. High cortisol levels d. High incidence of substance abuse Answer: c Textbook Reference: Characteristics of Anxiety Disorders 25. Which statement about OCD is false? a. It is characterized by obsessions and compulsions. b. It is now considered to be the most common anxiety disorder. c. It creates great anxiety for patients if they are unable to carry out their rituals.

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d. It is considered by some researchers to be a motor disorder.

Answer: b Textbook Reference: Characteristics of Anxiety Disorders 26. All of the following brain areas have been implicated in the neurobiological model of OCD except for the a. amygdala. b. basal ganglia. c. thalamus. d. anterior cingulate cortex.

Answer: a Textbook Reference: Characteristics of Anxiety Disorders 27. The is believed to have a central role in the neurobiology associated with the characteristic repetitive and ritualistic thoughts associated with OCD. a. substantia nigra b. hippocampus c. caudate nucleus d. primary motor cortex Answer: c Textbook Reference: Characteristics of Anxiety Disorders 28. Drugs that relieve anxiety are a. anxiolytics. b. sedatives. c. CNS depressants. d. All of the above Answer: d Textbook Reference: Characteristics of Anxiety Disorders 29. Anxiolytic drugs do not a. produce relaxation along with drowsiness and poor motor coordination. b. typically cause their effects on the CNS by increasing the transmitter dopamine. c. include alcohol which has a very unsafe therapeutic index. d. reduce seizures.

Answer: b Textbook Reference: Characteristics of Anxiety Disorders 30. Which of the following is not a way that benzodiazepines affect GABA at the synapse? a. They act as GABA antagonists and produce inhibitory effects. b. They cause an IPSP. c. They result in a local hyperpolarization. d. They cause the chloride ion channel to open more frequently.

Answer: a Textbook Reference: Drugs for Treating Anxiety, OCD, and PTSD

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31. While barbiturates are probably the oldest of the sedative hynotics, they are not currently used for anxiety/insomnia because a. sodium amytal was the only barbiturate available. b. barbiturates only came in short-acting forms. c. barbiturates can be lethal, while benzodiazepenes are much safer. d. barbiturates do not help with insomnia.

Answer: c Textbook Reference: Drugs for Treating Anxiety, OCD, and PTSD 32. Which of the following is not a side effect of the barbiturates? a. Tolerance to the sedative effects of the drug b. REM rebound after withdrawal from the medication c. Cognitive deficits d. Tolerance to the respiratory effects of the drug Answer: d Textbook Reference: Drugs for Treating Anxiety, OCD, and PTSD 33. Tolerance develops to the effects of barbiturates, but not to the effects. a. sedative; respiratory-depressant b. muscle relaxant; mood c. respiratory-depressant; hypnotic d. reinforcing; sedative Answer: a Textbook Reference: Drugs for Treating Anxiety, OCD, and PTSD 34. Which of the following is not a reason that the benzodiazepines are preferred over barbiturates? a. They do not produce much sedation. b. They have a low incidence of tolerance. c. There is a less severe withdrawal syndrome. d. They are more effective at reducing anxiety.

Answer: d Textbook Reference: Drugs for Treating Anxiety, OCD, and PTSD 35. The duration of action of benzodiazepines a. is fairly constant, ranging from 10–20 hours. b. is longer for drugs like Valium and Librium that have active metabolites. c. depends partly on whether drugs are redistributed to fat and muscle depots. d. is equal to the length of time it takes for phase I metabolism to occur.

Answer: c Textbook Reference: Drugs for Treating Anxiety, OCD, and PTSD 36. All of the following are therapeutic uses of the benzodiazepines except a. presurgical anesthesia involving relaxation and decreased awareness.

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b. treatment of insomnia. c. muscle relaxation. d. deep anesthesia involving loss of consciousness.

Answer: d Textbook Reference: Drugs for Treating Anxiety, OCD, and PTSD 37. Which of the following is not an advantage that the benzodiazepines have over the barbiturates? a. There is more metabolic tolerance with the benzodiazepines than the barbiturates. b. The benzodiazepines have a higher therapeutic index. c. There is an antagonist drug available to reverse the effects of benzodiazepine overdose but not barbiturate overdose. d. The withdrawal syndrome following use of benzodiazepines is milder than that of the barbiturates, and it is not life-threatening.

Answer: a Textbook Reference: Drugs for Treating Anxiety, OCD, and PTSD 38. If individuals experience an abstinence syndrome when withdrawing from benzodiazepenes, one would expect to see a. a withdrawal syndrome that is life threatening. b. a milder withdrawal syndrome than one following ethanol or barbiturate withdrawal. c. a more severe withdrawal syndrome than barbiturates. d. symptoms that include increased sleepiness and mania.

Answer: b Textbook Reference: Drugs for Treating Anxiety, OCD, and PTSD 39. BuSpar or buspirone has all of the following effects except a. it is more effective at reducing the cognitive aspects of worry than the physical components of anxiety. b. it is a partial agonist at the benzodiazepine receptor. c. it does not cause sedation or confusion. d. it is unlikely to be abused as it may cause dysphoria.

Answer: b Textbook Reference: Drugs for Treating Anxiety, OCD, and PTSD 40. Which of the following is not a reason BuSpar has limitations as a clinically effective drug? a. It takes too long to work; hence it cannot be used for situational anxiety. b. It shows no cross-tolerance with other sedative-hypnotics and hence cannot be used to substitute for these drugs during withdrawal. c. It is not useful as a treatment for insomnia. d. It produces a severe withdrawal syndrome.

Answer: d Textbook Reference: Drugs for Treating Anxiety, OCD, and PTSD 41. BuSpar’s therapeutic effects are related to its actions on

receptors.

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a. GABA A b. 5-HT2A c. 5-HT1A d. both GABA A and GABA B Answer: c Textbook Reference: Drugs for Treating Anxiety, OCD, and PTSD 42. Which of the following is not a reason that antidepressants are used to treat anxiety disorders? a. Depression and anxiety often occur together in the same person. b. The side effects of the SSRIs are more tolerable than those of the anxiolytic drugs. c. The antidepressant desipramine is particularly effective in treating all forms of anxiety and depression. d. Some people with anxiety disorders are prone to drug abuse and should not take the traditional anxiolytics; antidepressants are another option.

Answer: c Textbook Reference: Drugs for Treating Anxiety, OCD, and PTSD 43. One significant problem with using antidepressants to relieve anxiety is that antidepressants a. like SSRIs can take 4–6 weeks to work. b. like SSRIs have more significant side effect profiles than all other anxiolytic drugs. c. like barbiturates do not relieve anxiety. d. do not work on anxiety.

Answer: a Textbook Reference: Drugs for Treating Anxiety, OCD, and PTSD

Short Answer/Essay 44. Explain how anxiety can be both important and maladaptive for survival. In your answer describe the three-component model of anxiety.

Answer: Anxiety can have an important role in survival by warning us about danger and activating the sympathetic nervous system to help us cope with impending danger or emergencies. However, too much anxiety can have adverse effects and impair our ability to perform appropriately. The three-component model of anxiety includes a cyclical interaction of bodily responses, ineffective behaviors, and upsetting thoughts. Each of these three components can influence the others, resulting in an escalating overall damaging effect of too much anxiety. Some individuals perceive stressors as a challenge that results in improved performance; others get overwhelmed and focus only on failure.

Textbook Reference: Neurobiology of Anxiety 45. Compare and contrast fear and anxiety with respect to their triggering events, and their neurobiology.

Answer: Anxiety has to do with apprehension about possible future events or misfortune and concern about how to deal with it or the ability to predict it. In contrast, fear is an

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emotional response to danger and occurs when you are confronted. It is characterized by a strong urge to escape. The amygdaloid complex plays a major role in anxiety-related information processing by several brain regions. There are a number of components as part of these behaviors in addition to the amygdala including the limbic cortex, the hypothalamus, and the hippocampus. The amygdala receives sensory and cognitive information from the sensory thalamus, sensory, and association cortices and hippocampus; these brain areas project to the lateral nucleus of the amygdala. From the lateral nucleus of the amygdala it goes to the central nucleus (through direct and indirect connections and the bed of the stria terminalis which innervates widespread brain regions to orchestrate emotions. Fear is orchestrated by the central nucleus of the amygdala resulting in ANS activation, enhanced reflexes, activation of the HPA, etc.

Textbook Reference: Neurobiology of Anxiety 46. Describe an animal model used to study anxiety.

Answer: Knockout mice lacking the 5-HT1A receptor represent a genetic model of anxiety, demonstrated by increased anxious behaviors in the light–dark, open field, elevated plus-maze, and novel object tests. All of these behavioral tests tap into models of anxiety in rodents.

Textbook Reference: Neurobiology of Anxiety 47. Identify the major brain regions that are involved in anxiety. What area plays a coordinating role? Cite evidence that shows GABA is involved in these pathways.

Answer: The amygdaloid complex within the temporal lobes plays an important role in emotional processing. The circuits include limbic cortex (insula and anterior cingulate cortex [ACC]), hypothalamus, and hippocampus. These circuits respond to environmental stimuli, cognitions, etc., and are activated from sensory thalamus, sensory and association cortex, and hippocampus. These regions project to the amygdala, and imaging studies suggest that we see activation during anxiety and fear. GABA plays a major role in modulating anxiety. GABA helps regulate the activation of the central nucleus of the amygdala as well as GABA-induced inhibition of local circuits. Glutamatergic neurons from the PFC stimulate GABA neurons in the amygdala to provide a top-down level of control. Drugs that reduce anxiety, particularly the benzodiazepenes, modulate GABA activity, working on the GABA A receptor. Direct administration of GABA or GABA agonists into the amygdala has anxiolytic effects in many rodent models of anxiety.

Textbook Reference: Neurobiology of Anxiety 48. Describe the way that CRF acts as both a hormone and a neurotransmitter to coordinate the brain’s response to stressors.

Answer: CRF acts as a hormone and is released from the paraventricular nucleus of the hypothalamus during stress. This travels to the anterior pituitary to release the stress hormone adrenocorticotropic hormone (ACTH) into the blood, which in turn increases the release of glucocorticoids such as cortisol from the adrenal cortex. Direct neuronal application of CRF produces strong excitatory effects in many brain areas that contain significant numbers of CRF receptors, including the hippocampus, amygdala, LC, cortex, and hypothalamus, all of which are parts of the neural circuit for anxiety. Of particular

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significance are the large numbers of CRF nerve endings and CRF receptors found in the amygdala.

Textbook Reference: Neurobiology of Anxiety 49. Give four types of evidence that suggest that norepinephrine plays a central role in the expression and treatment of anxiety disorders.

Answer: Evidence includes: • Animals exposed to novel stimuli that signal stress increase electrical activity and enhance expression of the immediate early gene c-fos, an indicator of neuroneal activation in LC. • Electrical stimulation of LC or administration of an α2 -autoreceptor antagonist yohimbine (which increases NE release) induces a wide range of alerting and fear responses.

• Yohimbine also produces panic attacks in patients with PTSD or panic disorder.

• Some of the therapeutic effects of anxiolytic drugs can be explained by modulation of LC firing. Noradrenergic cells in the LC are excited by CRF synaptic input and are inhibited by γ-aminobutyric acid (GABA) and serotonin (5HT), as well as by stimulation of α2 -adrenergic somatodendritic autoreceptors.

Since benzodiazepines enhance the inhibitory function of GABA, reduced LC firing may be responsible for at least some of the anxiolytic effects of these drugs.

A similar argument is used for some of the antidepressents that appear effective in treating certain types of anxiety (inhibiting LC firing).

Textbook Reference: Neurobiology of Anxiety 50. Explain the effects of agonists, inverse agonists, and antagonists at the benzodiazepine site on GABA receptor function and on anxiety. How do the neuroactive steroids affect GABA receptors?

Answer: Agonists such as benzodiazepenes bind to a distinct modulatory site on the GABA receptor which enhances GABA binding. Flumazenil prevents the effects of BDZ binding but has no effect on the GABA receptor, so serves as a BDZ antagonist. There are also drugs that bind to the BDZ site and act as inverse agonists, producing effects that are opposite of BDZ drugs (e.g., anxiety). Neurosteroids also have a modulatory site on GABA A receptors and when they bind to their modulatory site, they enhance GABAinduced chloride influx.

Textbook Reference: Drugs for Treating Anxiety, OCD, and PTSD 51. Explain the evidence supporting a role for both genes and environment (especially exposure to early stress) in the expression of anxiety. Include physiological and behavioral findings in your answer. How are epigenetic factors involved?

Answer: Animal and human studies have shown that early exposure to stress and neglect can alter the developing brain and can produce a lifelong change in response to stressors, resulting in enhanced anxiety. Early stress can produce behaviors resembling anxiety, including hyperarousal, enhanced freezing, increased fear-potentiated startle, etc. Early stress can also alter programing of the HPA axis, resulting in a hyperactive hormonal response to challenge that persists into adulthood. That these changes persist into adulthood suggests that epigenetic factors play a role.

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Textbook Reference: Neurobiology of Anxiety 52. Name and describe the principal clinical anxiety disorders. For each, indicate risk factors and general treatments if known.

Answer: The main clinical anxiety disorders are: • Generalized anxiety disorder (GAD): one of the more common anxiety disorders; individuals show constant signs of worry. Mixed data regarding whether there is a genetic predisposition. Associated with enlargement and hyperactivity of the amygdala with too little inhibitory control by the PFC. Symptoms are reduced by drugs that enhance GABA function like benzodiazepenes.

• Panic attacks and panic disorders with anticipatory anxiety: this is more of a fear reaction; accompanied by strong arousal of the sympathetic nervous system.

Symptoms can last for minutes or sometimes hours. Can be brought on by an environmental cue or can occur entirely without warning. During a panic attack, neural activity is increased in amygdala, cingulate cortex, and insula, and reduced in PFC. Genetic predisposition for panic disorders. Drugs that reduce NE seem to have an anxiolytic effect; behavioral desensitization also works.

• Phobias: fears of specific objects or situations; individual recognizes them as irrational. Can impact quality of life. Can usually be effectively treated with behavior therapy that involves gradual desensitization (behavioral desensitization). Medication is rarely needed.

• Social anxiety disorder: most common; fear of being evaluated or criticized.

SSRIs and cognitive therapy work best. Onset is typically at a younger age.

Slightly more common in women and in individuals with low self-esteem. SSRIs and behavior therapy can work. BDZs and β-adrenergic blocks can reduce autonomic nervous systems can help reduce symptoms.

• Post-traumatic stress disorder: severe and chronic emotional disorder after traumatic events. Can include nightmares, memories that may occur as sudden flashbacks of traumatic events. May be a genetic risk for likelihood of developing PTSD. Low blood cortisol may be a make of vulnerability for PTSD. Exposure therapy is a cognitive therapy that is somewhat effective.

• Obsessive-compulsive disorder: recurring thoughts and behaviors that incapacitate and interferes with normal daily function. The caudate nucleus has a central role in the pathophysiology of OCD and is one component in the dysfunctional cortico-striatal-thalamic-cortical loop. SSRIs are somewhat successful. Behavioral therapy is also effective.

Textbook Reference: Characteristics of Anxiety Disorders 53. Describe the incidence of PTSD; and explain the relationship between occurrence of PTSD and type of trauma, genetic factors, and cortisol levels.

Answer: PTSD estimates range from 1–10% prevalence in the U.S. It is a severe emotional disorder that can occur after traumatic events. PTSD is related to the intensity of the trauma but not all individuals develop PTSD. There does seem to be a genetic component for risk of developing PTSD. Family studies suggest that many people who develop PTSD after trauma have a family history of some type of psychopathology, and there is a higher concordance rate among monozygotic twins. There may be a gender

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difference as well, with women showing an increased incidence of PTSD. Some studies suggest that patients with PTSD have a lower than normal level of blood cortisol (associated with increases in CRF and NE). Some researchers think that this lower cortisol could be a risk factor for who is more likely to develop PTSD. Textbook Reference: Characteristics of Anxiety Disorders 54. Describe the general classification, characteristics, and uses of anxiolytic drugs.

Answer: Drugs that relieve anxiety are called anxiolytic drugs. Many of these belong to the class of sedative hypnotics. These drugs reduce anxiety, produce a calm and relaxed state, and at higher doses can produce incoordination, mental clouding, and can induce sleep. At extremely high doses, some of these CNS depressants can induce coma and death. Certain sedative hypnotics have anticonvulsant properties; others can be used to reduce muscle spasms. The main mechanism of action of the anxiolytics is to enhance GABA neurotransmission.

Textbook Reference: Drugs for Treating Anxiety, OCD, and PTSD 55. Identify several therapeutic uses for the benzodiazepine drugs. Give three reasons for preferring benzodiazepines over barbiturates as anxiolytics.

Answer: Benzodiazepenes have a number of therapeutic uses. Short-acting benzodiazepenes can be used as presurgical anesthetics—they can be used to reduce stress prior to a diagnostic or dental procedure. They are excellent anxiolytics and can be used to help promote sleep (although this is not a good choice long-term). Some are excellent as muscle relaxants; some are anticonvulsants and can be very useful with detoxification during ethanol withdrawal. They are considerably safer, have less serious withdrawal, and produce less tolerance than barbiturates.

Textbook Reference: Drugs for Treating Anxiety, OCD, and PTSD 56. Explain how barbiturates and benzodiazepines affect the GABA receptor complex.

How does this relate to their clinical efficacy?

Answer: Benzodiazepines and barbiturates both produce their effects by binding to distinct modulatory sites different from the GABA binding site on the receptor complex.

In contrast with BDZs, barbiturates increase the duration of the opening of GABAactivated Cl– channels rather, than the number of openings. Barbiturates also directly open the Cl– channel without GABA. This additional action may explain why barbiturates can be lethal but benzodiazepines are not.

Textbook Reference: Drugs for Treating Anxiety, OCD, and PTSD 57. Describe the unique clinical and synaptic effects of the drug BuSpar. What are its advantages and disadvantages over the benzodiazepines?

Answer: Buspar has a novel structure and mechanism of action compared with the sedative–hypnotics. Unlike the sedative–hypnotics, it does not enhance GABA function but instead acts as a partial agonist at serotonergic 5-HT1A receptors. The neurochemical basis of the anxiolytic action of buspirone is not fully understood, but its partial agonist action at 5-HT1A receptors is the likely mediator of the drugs’ effectiveness. Its delayed onset of action would lead one to believe synaptic plasticity is necessary. Buspirone has several advantages over the benzodiazepines, including its usefulness in treating

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depression that often accompanies anxiety. In addition, its anxiety reduction is not accompanied by sedation, confusion, or mental clouding. Buspirone does not enhance the CNS-depressing effects of alcohol or other CNS depressants, so it is still safer than the BDZs. It also has a minimum of severe side effects, and fatalities have not been reported.

Further, it has little or no potential for recreational use or dependence. In fact, some patients report a dysphoric effect, described as a feeling of restlessness and malaise.

Finally, no rebound withdrawal syndrome has been reported for buspirone.

Textbook Reference: Drugs for Treating Anxiety, OCD, and PTSD

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Test Bank to accompany

Psychopharmacology, Third Edition Meyer • Quenzer

Chapter 18: Affective Disorders: Antidepressants and Mood Stabilizers Multiple Choice 1. Which statement about affective disorders is false? a. They are among the most common forms of mental illness. b. They date back to the time of ancient Greece and Hippocrates. c. They are linked more to environmental causes than to brain factors. d. They include major depression and bipolar disorder.

Answer: c Textbook Reference: Characteristics of Affective Disorders 2. Reactive depression a. typically results in anhedonia and feelings of worthlessness. b. leads to such loneliness that the person considers suicide as the only option. c. is one of the more serious affective disorders. d. often occurs following loss, failure, or disappointment.

Answer: d Textbook Reference: Characteristics of Affective Disorders 3. All of the following are symptoms of major depression except a. loss of appetite. b. dulled sense of pain. c. insomnia. d. agitation.

Answer: b Textbook Reference: Characteristics of Affective Disorders 4. Depression a. is most likely to recur following a period of stress. b. affects men and women equally. c. will not improve on its own; therapy is required. d. affects approximately 15% to 20% of the population at any given time.

Answer: d Textbook Reference: Characteristics of Affective Disorders 5. Which of the following is not a symptom of mania? a. Decrease in goal-directed activity b. Flight of ideas

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c. Distractability d. Elation Answer: a Textbook Reference: Characteristics of Affective Disorders 6. Which statement about bipolar disorder is false? a. It involves cycles of depression and mania that persist throughout the life span. b. It can provide times of creativity and productivity if the energy during the manic periods is channeled appropriately. c. It occurs in about 10% of the population. d. It affects men and women between the ages of 20 and 30 equally.

Answer: c Textbook Reference: Characteristics of Affective Disorders 7. Which statement about risk factors for mood disorders is false? a. Psychiatric disorders develop in response to the interaction of genes and environmental events. b. For affective disorders, environmental triggers alone are enough to cause serious mood changes. c. The genetic factors involved in mood disorders indicate that the individual will be more susceptible to the disorder, not that they will definitely develop it. d. Environmental stress is a likely risk factor for mood disorders.

Answer: b Textbook Reference: Characteristics of Affective Disorders 8. Which statement about the role of heredity in the affective disorders is true? a. No single dominant gene for these disorders has yet been identified. b. Adoption studies provide the strongest evidence for a genetic basis to the affective disorders. c. Twin studies show that the monozygotic-dizygotic twin difference in concordance rates is greater for severe depression than for bipolar disorder. d. Linkage studies attempt to study the incidence of a disorder in an extended family.

Answer: a Textbook Reference: Characteristics of Affective Disorders 9. Which statement about stress is false? a. It often precedes the first episode of depression b. Depressed patients have altered stress hormone levels c. Researchers can describe a typical ―stress response‖ because everyone responds to life stresses in pretty much the same way d. The involvement of stress is one factor that links the disorders of depression and anxiety together Answer: c Textbook Reference: Characteristics of Affective Disorders

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10. Which event does not occur during stress activation of the hypothalamic–pituitary– adrenal (HPA) axis? a. NE and ACh regulate the release of corticotrophin-releasing factor (CRF) from the hypothalamus. b. ACTH causes the release of cortisol from the adrenal gland. c. Cortisol feeds back to shut down HPA activation. d. Glucocorticoids feedback to stimulate the hippocampus.

Answer: d Textbook Reference: Characteristics of Affective Disorders 11. Researchers know that depressed individuals have an abnormal stress response involving the HPA axis because these individuals have all of the following except a. elevated levels of cortisol. b. shrunken pituitary and adrenal glands. c. higher CRF levels in cerebrospinal fluid (CSF). d. more CRF cells evident in postmortem hypothalamic tissue.

Answer: b Textbook Reference: Characteristics of Affective Disorders 12. What is a dexamethasone challenge? a. Depressed individuals are given a synthetic glucocorticoid to see if it shuts the HPA axis down. b. Depres sed patients are given a synthetic CRF to try to ―jump start‖ the HPA axis. c. Depressed individuals are given a form of ACTH to shut the HPA axis down and allow it time for recovery from stress over-responding. d. Depressed patients are given a glucocorticoid blocker to regulate an out-of-control system.

Answer: a Textbook Reference: Characteristics of Affective Disorders 13. Which of the following is not a sleep abnormality experienced by depressed individuals? a. Significant decrease in stages 3 and 4 slow-wave sleep b. Earlier onset of REM sleep c. Increased REM in the first third of the night d. Rapid sleep onset Answer: d Textbook Reference: Characteristics of Affective Disorders 14. All of the following are characteristic of sleep abnormalities in depression except a. longer time for sleep onset. b. earlier onset of REM sleep. c. longer REM periods as sleep progresses. d. frequent awakenings from sleep.

Answer: c Textbook Reference: Characteristics of Affective Disorders

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15. Recently developed models of mania include and the creation of mutant mice targeting genes involved in . a. sleep deprivation; serotonin synthesis b. maternal separation; lithium resistance c. sleep deprivation; the circadian clock d. chronic mild stress; lithium sensitivity Answer: c Textbook Reference: Animal Models of Affective Disorders 16. The monoamine hypothesis is supported by all of the following findings except a. the drug reserpine depletes vesicles of monoamine transmitters and causes depression. b. people with depression have extraordinarily high levels of MHPG and 5-HIAA in their urine, blood, and CSF. c. TCAs reverse symptoms of depression. d. MAOIs reverse symptoms of depression.

Answer: b Textbook Reference: Neurochemical Basis of Mood Disorders 17. Which statement about new research into biochemical models for mood disorders is false? a. The monoamine hypothesis needs to be updated with information that explains the slow onset of the clinical effects of the drugs. b. PET scans and MRI can be used to discriminate between people with and without mood disorders in order to contribute to new models. c. Animal models are no longer useful in the search for modern biochemical models for human conditions. d. New models will have to consider multiple neurotransmitter systems and how they interact.

Answer: c Textbook Reference: Neurochemical Basis of Mood Disorders 18. Which research finding does not confirm a role for serotonin dysfunction in mood disorders? a. Decreased numbers of postsynaptic 5-HT2 receptors are found in depressed patients. b. Low 5-HIAA turnover is found in depressed individuals. c. Rapid tryptophan depletion in treated depressed patients causes a relapse in symptoms. d. Challenge studies indicate that the 5-HT receptors in depressed individuals are less sensitive.

Answer: a Textbook Reference: Neurochemical Basis of Mood Disorders 19. Animal studies of the acute and chronic effects of antidepressants on serotonin have shown all of the following except a. the autoreceptors are activated acutely, causing a decrease in synthesis and release of 5-HT.

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b. the reuptake transporters remain blocked for the duration of the drug’s action. c. tolerance to the drug occurs at the autoreceptors chronically, resulting in increased 5HT release. d. setotonin occupancy of serotonin autoreceptors activates cell firing following chronic antidepressant treatment Answer: d Textbook Reference: Neurochemical Basis of Mood Disorders 20. Which statement regarding the glucocorticoid hypothesis of depression is false? a. The amygdala normally inhibits the hypothalamic–pituitary–adrenal axis, whereas the hippocampus activates it. b. High cortisol levels cause loss of cells as well as reduced neurogenesis in the hippocampus. c. Behavior characteristic of depression can be elicited in animals by administration of CRF. d. ECT and antidepressant drugs may exert some of their clinical benefits by decreasing CRF. Answer: a Textbook Reference: Neurobiological Models of Depression 21. The neurotrophic hypothesis of depression is supported by all of the following except a. chronic stress decreases hippocampal brain-derived neurotrophic factor (BDNF). b. acute antidepressant treatment protects neurons by increasing BDNF. c. chronic antidepressant treatment increases BDNF in both humans and animals. d. BDNF is enhanced by upregulation in the cAMP cascade, as occurs with treatments for depression.

Answer: b Textbook Reference: Neurobiological Models of Depression 22. Chronic social defeat stress causes an increase in histone , which leads to a decrease in BDNF gene expression by tightening the structure of chromatin.

Antidepressant treatment results in a(n) and enhanced BDNF expression. a. acetylation; decrease in histone acetylation b. acetylation; increase in histone methylation c. methylation; decrease in histone methylation d. methylation; increase in histone acetylation Answer: d Textbook Reference: Neurobiological Models of Depression 23. Which of the following is/are not primarily used for treating major depression? a. Selective serotonin reuptake inhibitors (SSRIs) b. Lithium therapy c. Monoamine oxidase inhibitors (MAO-Is) d. Atypical antidepressants Answer: b Textbook Reference: Therapies for Affective Disorders

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24. Which statement concerning the use of antidepressant medication in general is true? a. Placebo-controlled studies show that antidepressant medications are effective in about 80% of the people that use them for depression. b. Antidepressant drugs have predictable outcomes and side effects that make it relatively easy for a psychiatrist to choose a medication for a given patient. c. The therapeutic effects of antidepressants involve changes in the brain that can take up to several weeks to develop. d. The maintenance period of drug treatment should be no longer than 4 to 5 months.

Answer: c Textbook Reference: Therapies for Affective Disorders 25. Which MHPG about MAO inhibitors is false? a. The first MAOI, iproniazid, was discovered by accident while investigating treatments for tuberculosis. b. They can be used safely with proper dietary restrictions. c. They block the metabolism of norepinephrine, dopamine, and serotonin. d. These drugs have little use in the treatment of depression given the availability of safer drugs, and no use in the treatment of other disorders.

Answer: d Textbook Reference: Therapies for Affective Disorders 26. What effect of MAOIs at the synapse is correlated with their therapeutic effectiveness? a. The enzyme MAO is inhibited, elevating the amount of transmitters available for release. b. The normal amount of transmitter in the presynaptic terminal is properly regulated by the drug, which acts as an enzyme. c. The synapse adapts by increasing receptors for the amine transmitters. d. Postsynaptic changes occur in second-messenger systems, up-regulating cAMP. Answer: d Textbook Reference: Therapies for Affective Disorders 27. Which of the following is not a problem or side effect of MAOIs? a. Enhanced activity of cytochrome P450 enzymes b. Overeating of carbohydrates c. Interaction with drugs that affect the sympathetic nervous system d. Elevated tyramine levels when combined with certain foods Answer: a Textbook Reference: Therapies for Affective Disorders 28. All of the following are foods that should be avoided by people taking MAOIs except a. aged cheese. b. eggs. c. wine. d. yeasty breads.

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Answer: b Textbook Reference: Therapies for Affective Disorders 29. Which statement about tricyclic antidepressants is false? a. They enhance the function of the presynaptic transporter protein for serotonin and/or norepinephrine. b. They cause long-term adaptive changes at the synapse that are related to their therapeutic effects. c. They affect acetylcholine, histamine, and α-adrenergic receptors. d. They include the prototype imipramine, which resembles drugs in the phenothiazine class of antipsychotics.

Answer: a Textbook Reference: Therapies for Affective Disorders 30. All of the following are potential side effects of the tricyclic antidepressants except a. sedation. b. confusion. c. hypertension. d. urinary retention.

Answer: c Textbook Reference: Therapies for Affective Disorders 31. The greatest danger of the tricyclic antidepressants is a. stroke. b. cardiac arrest. c. psychosis. d. migraine.

Answer: b Textbook Reference: Therapies for Affective Disorders 32. What is the major advantage of the second-generation antidepressants over the MAOIs and the TCAs? a. They are more effective in treating depression. b. They work faster than the older classes of drugs. c. They produce different and less harmful side effects than the older medications. d. They are less selective in their action; hence they can be used for a number of conditions.

Answer: c Textbook Reference: Therapies for Affective Disorders 33. All of the following are side effects of the selective serotonin reuptake inhibitors (SSRIs) except a. blurred vision. b. insomnia. c. headache. d. movement disorders.

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Answer: a Textbook Reference: Therapies for Affective Disorders 34. Which side effect is a frequent reason for individuals terminating SSRI use? a. Anxiety b. Insomnia c. Sexual dysfunction d. Muscle rigidity Answer: c Textbook Reference: Therapies for Affective Disorders 35. Which statement about serotonin syndrome is false? a. It can occur when SSRIs are combined with other serotonin agonists. b. It is characterized by agitation and disorientation. c. Symptoms include exaggerated autonomic nervous system activity. d. While frightening, the syndrome is not life-threatening.

Answer: d Textbook Reference: Therapies for Affective Disorders 36. would be considered a third-generation antidepressant. a. Remeron, a dual NE/5-HT modulator b. Zoloft c. CRF receptor antagonist d. Wellbutrin Answer: c Textbook Reference: Therapies for Affective Disorders 37. Which statement regarding intravenous ketamine as a treatment for depression is false? a. The dose required to reduce depression symptoms is much higher than that needed for anesthesia. b. It reduces symptoms in 65–70% of patients who are resistant to other treatments. c. Its effects typically last 1–3 weeks. d. In addition to blocking NMDA type glutamate receptors, it enhances AMPA receptor response to glutamate.

Answer: a Textbook Reference: Therapies for Affective Disorders 38. Which statement about lithium is false? a. It reduces manic symptoms in about 60–80% of cases. b. It is taken for the maintenance period of 6–8 months and should then be safely withdrawn. c. It is often administered with an antidepressant drug. d. It dramatically increases the time between recurring episodes of mania and depression.

Answer: b Textbook Reference: Therapies for Affective Disorders

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39. Which of the following is not a way that lithium acts on the synapse? a. Increases catecholamine activity b. Increases 5-HT and 5-HIAA c. Affects second-messenger systems d. Influences brain neurotrophic factors Answer: a Textbook Reference: Therapies for Affective Disorders 40. Which of the following is not a side effect of lithium? a. Increased thirst and urination b. Impaired concentration and memory c. Anxiety d. Weight gain Answer: c Textbook Reference: Therapies for Affective Disorders 41. All of the following are alternatives to lithium as treatments for bipolar disorder except a. Tegretol. b. Gabitril. c. Depakote. d. L-DOPA. Answer: d Textbook Reference: Therapies for Affective Disorders

Short Answer/Essay 42. Distinguish between reactive depression, major depression, and bipolar disorder in terms of symptoms and incidence.

Answer: Reactive depression is sadness that results from negative events in life, such as death of a loved one, which everyone experiences, and is not considered a mental disorder. Major depression, also known as unipolar depression, involves recurring periods of sadness, hopelessness, and guilt. Incidence is about a 3% lifetime risk for men and about 6% for women. Bipolar disorder involves an alteration between periods of depression and periods of mania (extreme elation, confidence to the point of overconfidence, impulsive decision making), with an incidence of about 1% in both men and women.

Textbook Reference: Characteristics of Affective Disorders 43. Evaluate the role of the following risk factors in depression: hereditary factors, stress, and biological rhythms. Briefly discuss the role of melatonin receptor therapy for depression as it relates to altered biological rhythms.

Answer: Genetics can play a significant role in depression, with identical twin studies indicating a concordance rate of over 50%. The fact that this is not 100% indicates that

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environmental factors, such as stress, can also contribute to the probability of depression occurring. And genetic factors can also influence how an individual responds to life stresses. Abnormal levels of cortisol secretion may occur in depressed individuals, as well as abnormal rhythms of circulating cortisol and sleep patterns. Since melatonin has been implicated in affecting body rhythms, melatonin therapy has been used in an attempt to normalize body rhythms, such as sleep patterns.

Textbook Reference: Characteristics of Affective Disorders 44. What is the dexamethasone test for cortisol levels, and what is its significance?

Answer: This test measures the inhibition of cortisol secretion following administration of the synthetic glucocorticoid, dexamethasone (a form of feedback inhibition that normally occurs). In some depressed patients there is a blunted inhibition, and it has been suggested that those with a blunted inhibition response may be more likely to have a depression relapse.

Textbook Reference: Characteristics of Affective Disorders 45. Why is the Clock protein of interest in studies on bipolar disorder?

Answer: The Clock protein is involved in regulating circadian rhythms, and circadian rhythms are often abnormal in patients with bipolar disorder. Knocking out the gene that codes for the Clock protein in mice can also produce abnormalities in circadian rhythms.

Chronic treatment with lithium, which reduces manic symptoms in human bipolar patients, also reduces manic symptoms in the mice lacking the Clock protein. This provides a rationale for using the Clock protein deletion as a possible animal model for bipolar disorder.

Textbook Reference: Animal Models of Affective Disorders 46. Describe the monoamine hypothesis of mood disorders and several pieces of evidence that support it. In what ways is the hypothesis weak or incomplete?

Answer: The monoamine hypothesis of mood disorders suggests that a deficit in the functioning of monoamines such as serotonin and norepinephrine contributes to the production of depression. Evidence in favor includes the production of depression in some patients who have taken reserpine for treating high blood pressure. Reserpine depletes the stores of serotonin and norepinephrine by inhibiting their uptake into synaptic vesicles. Conversely, administration of a monoamine oxidase inhibitor (MAOI), which inhibits metabolism of biogenic amines, can cause an elevation in mood. Evidence against this hypothesis includes the observation that measurements of biogenic amine metabolites in cerebrospinal fluid (CSF), which can reflect biogenic amine activity in the brain, have not been consistent in showing differences between those with and without depression. Also, since drugs such as reserpine and MAOIs affect several biogenic amines (serotonin, dopamine, norepinephrine, epinephrine), specifying which transmitter(s) may be of special significance for depression would require additional studies.

Textbook Reference: Neurochemical Basis of Mood Disorders

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47. Describe evidence from studies measuring 5-HT turnover, tryptophan levels, receptor binding, and response to various drug challenges that supports a role for serotonin dysfunction in mood disorders.

Answer: Serotonin synthesis can be disrupted by giving animals an inhibitor of tryptophan hydroxylase, which is necessary for serotonin formation, or by using mice that have this enzyme deleted. Serotonin formation can also be altered by administering tryptophan (which will increase serotonin formation) or by feeding a diet low in tryptophan (this will lower serotonin levels). Receptor functioning can be altered by giving receptor antagonists (to block the receptors), or agonists (to activate the receptors), or by using mice who have a particular receptor subtype deleted. In animal studies, behavioral changes can be observed following an alteration in serotonin activity; for instance, an increase in aggression can occur following inhibition of serotonin functioning. In addition, altered eating patterns can be observed with serotonin manipulation. And in humans in remission, a low tryptophan diet can bring about a depression relapse.

Textbook Reference: Neurochemical Basis of Mood Disorders 48. Compare the acute and chronic effects of antidepressant drugs on the 5-HT synapse in order to explain why therapeutic efficacy takes several weeks to become evident.

Answer: Using a selective serotonin reuptake inhibitor (SSRI), such as fluoxetine (Prozac), as an example: An acute effect would be to inhibit serotonin reuptake from the synaptic cleft, and potentially provide more serotonin receptor activation. However, given the existence of presynaptic auto-inhibitory receptors that inhibit serotonin release, one may initially get a cancelling out of effects, so no net difference in serotonin activation of postsynaptic receptors occurs. With chronic administration, if the presynaptic receptors desensitize, then the net effect will be more serotonin activation of postsynaptic serotonin receptors. This could take several weeks to occur. This is just one theory about the time lag for the therapeutic effect of antidepressant drugs.

Textbook Reference: Neurochemical Basis of Mood Disorders 49. Name and describe the two neurobiological models of depression and provide supportive evidence for each. What types of novel treatments are suggested by these models?

Answer: One model suggests that abnormalities in CRF and/or cortisol functioning may lead to abnormally high levels of cortisol. This, in turn, could cause damage to brain areas such as the hippocampus, and could inhibit neurogenesis (new neuron formation) from occurring. If true, one type of treatment could involve the use of CRF receptor antagonist. Another model, possibility related to the abnormal cortisol model, suggests that a deficit in a neurotrophic factor, brain-derived neurotrophic factor (BDNF), may contribute to depressive symptomology. Since BDNF production is related to cyclic AMP activity, one therapeutic approach to potentially increase BDNF functioning would be to increase cyclic AMP activity, possibly by inhibiting the activity of cyclic AMP phosphodiesterase, the enzyme that metabolizes cyclic AMP. Textbook Reference: Neurobiological Models of Depression

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50. Describe the epigenetic changes produced by chronic stress and explain how these changes affect gene expression of BDNF. What might these findings tell us about the pathophysiology of mood disorders? What new treatments do these findings suggest?

Answer: Stress can increase methylation of histones, which makes them bind better to DNA and inhibit DNA transcription, and therefore lower the amount of mRNA produced for certain proteins. BDNF is one example. Chronic antidepressant treatment can increase DNA transcription by acetylating histones, making them bind less strongly to DNA. This would suggest that one way to increase transcription would be to administer a histone deacetylase inhibitor, which would help maintain the histones in an acetylated form.

Textbook Reference: Neurobiological Models of Depression 51. Identify the two older classes of medications used to treat major depression. Describe their mechanism of action at the synapse and their major side effects.

Answer: One of the older treatments involves the use of monoamine oxidase inhibitors (MAOIs). These compounds can inhibit the metabolism of biogenic amines such as dopamine, norepinephrine, epinephrine, and serotonin, and thus potentiate their action in the synaptic cleft. Since norepinephrine metabolism is inhibited, potentiated norepinephrine action in the periphery can contribute to increased blood pressure. In addition, foods associated with fermentation, such as wine and cheese, contain tyramine.

Tyramine is normally metabolized by MAO. But if MAO is inhibited, tyramine can enter nerve terminals and stimulate norepinephrine release in the periphery. This can increase heart rate and force of contraction and cause vascular smooth muscle to constrict around blood vessels; both of these effects can cause a dangerous increase in blood pressure.

Patients taking these drugs have to be careful with their diet. And MAOIs may also cause inhibition of some of the other drug metabolizing enzymes (the cytochrome P450 enzymes). Another older class of antidepressants would be the tricyclic antidepressants.

These compounds inhibit the reuptake of catecholamines and/or serotonin. The specificity depends upon the exact structure of the tricyclic compound. Some of these agents can also inhibit histamine receptors, causing sedation, and some can inhibit muscarinic receptors, causing dry mouth, dry eyes and constipation. Blockade of α 1 receptors on vascular smooth muscle can cause orthostatic hypotension (low blood pressure when rising from a laying or sitting position), and blockade of norepinephrine reuptake at the heart can cause unwanted cardiac stimulation and possibly arrhythmias.

Textbook Reference: Therapies for Affective Disorders 52. What two groups of drugs were discussed as examples of the second -generation antidepressants? How are they different from the older medications used for depression?

For each group, indicate the mechanism of action and the major side effects.

Answer: Second generation drugs would include the selective serotonin reuptake inhibitors (SSRIs). These drugs have a much lower ED 50 for inhibiting serotonin reuptake compared to inhibiting catecholamine reuptake. Many of the side effects of earlier drugs can be avoided, although they can have side effects such as anxiety, headache, insomnia, sexual dysfunction, and withdrawal symptoms. Dual NE/5-HT modulators have also been introduced as second-generation antidepressants, with the idea that potentiating both of these transmitters may be better than just potentiating one. Depending upon the particular

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drug, reuptake can be blocked, or autoreceptors on the presynaptic terminals may be blocked; either way, the transmitter action in the synaptic cleft should be potentiated.

Textbook Reference: Therapies for Affective Disorders 53. Describe the mechanism of action of at least three third -generation antidepressants.

Answer: Since cortisol levels may be elevated in depressed patients, CRF antagonists can represent a third-generation approach to treatment. This will blunt the cortisol release by blunting ACTH release. Increasing cAMP functioning would be another approach, in the hope of increasing levels of proteins such as BDNF. This could be done with a cyclic AMP phosphodiesterase inhibitor, which would reduce cyclic AMP metabolism. A third approach would be the use of ketamine as an antidepressant agent. A main pharmacological action of this compound is non-competitive blockade of the glutamate NMDA receptors.

Textbook Reference: Therapies for Affective Disorders 54. Describe the evidence supporting a role for glutamate receptors as targets for antidepressants.

Answer: A role for glutamate is suggested by the clinical improvements shown in depressed patients when given ketamine. Ketamine is a non-competitive blocker of the glutamate NMDA receptor. Some success has been reported with ketamine in treatmentresistant patients, with some patients showing improvement in less than two hours. One suggested mechanism for the rapid action of ketamine is that it may cause an activation of AMPA receptors, with subsequent activation of the mTOR protein kinase signaling pathway. This, in turn, may lead to structural changes, such as changes in spine density.

Textbook Reference: Therapies for Affective Disorders 55. Provide evidence that indicates lithium is a very effective drug for bipolar disorder.

How does it work at the synapse? Why must blood levels of lithium be monitored on a regular basis? Discuss what happens if levels are too high or too low.

Answer: Bipolar patients on lithium therapy spend an average of two weeks per year in the hospital, while those not on lithium spend an average of 8–13 weeks. Those not on lithium have, on average, a manic episode every nine months, and a depressive episode every 14 months, while those on lithium have a manic episode once in every nine years, and a depressive episode once in every four years. Effects that might contribute to therapeutic effect include an enhancement of serotonin activity and a reduction in catecholamine activity. Other possible mechanisms include inhibition of glycogen synthase kinase-3 (GSK-3), which might affect circadian rhythms, and inhibition of phosphoinositide cycling. The therapeutic index of lithium is low: therapeutic level of about 1.0 mM, and toxic effects produced at 2.0 mM. This low index requires monitoring of blood levels of lithium. Toxic effects can include cramps, diarrhea, vomiting, confusion, and at 3.0 mM, coma and death. Levels below 0.7 mM may not achieve therapeutic effectiveness.

Textbook Reference: Therapies for Affective Disorders

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Test Bank to accompany

Psychopharmacology, Third Edition Meyer • Quenzer

Chapter 19: Schizophrenia: Antipsychotic Drugs Multiple Choice 1. Psychoses are characterized by all of the following except a. severe distortions of reality. b. affective disturbances. c. problems with intellectual functioning. d. savant-like increases in intelligence.

Answer: d Textbook Reference: Characteristics of Schizophrenia 2. Concerning the incidence and severity of schizophrenia, a. although treatment is available, about 50% of people with the disorder spend a large part of their lives in mental hospitals. b. approximately 5% of the general population will receive a diagnosis of schizophrenia at some point in their lifetimes. c. the disorder is considered to be chronic and incurable. d. the incidence of the disorder is highest among young women in their late teens and early twenties.

Answer: c Textbook Reference: Characteristics of Schizophrenia 3. Which of the following is/are not a typical symptom of schizophrenia? a. Auditory hallucinations b. Delusions of persecution c. Vague or illogical speech d. Severe anxiety Answer: d Textbook Reference: Characteristics of Schizophrenia 4. Which statement regarding the diagnosis of schizophrenia is false? a. Clinicians do not agree on whether it is a single disorder or a group of disorders. b. The severity of the disorder and unusual symptoms make diagnosis straightforward. c. Diagnosis is complicated because symptoms of the disorder change over time. d. There are several subtypes of schizophrenia recognized by DSM-IV, making the task more complex.

Answer: b Textbook Reference: Characteristics of Schizophrenia

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5. Which of the following is not a subtype of schizophrenia, according to Kraepelin? a. Catatonic b. Delusional c. Undifferentiated d. Paranoid Answer: b Textbook Reference: Characteristics of Schizophrenia 6. According to the positive/negative symptom classification scheme for schizophrenia, a. people with positive symptoms have a poor outcome as they do not respond well to medications. b. positive symptoms are made worse by drugs that increase dopamine. c. people with negative symptoms tend to develop their problems in adulthood. d. delusions and hallucinations are examples of negative symptoms.

Answer: b Textbook Reference: Characteristics of Schizophrenia 7. The symptoms of schizophrenia that tend to be more difficult to treat are a. the positive symptoms. b. the positive and the negative symptoms. c. the negative symptoms and the cognitive symptoms. d. the cognitive symptoms and the positive symptoms.

Answer: c Textbook Reference: Characteristics of Schizophrenia 8. Which of the following are not structural changes observed in the brains of people with schizophrenia? a. Reduced volume of the temporal lobe and limbic structures b. Shrinkage of the ventricles c. Atrophy of selected cortical layers d. Disorganized arrangement of hippocampal cells Answer: b Textbook Reference: Characteristics of Schizophrenia 9. The most consistent functional abnormality in the brains of individuals with schizophrenia is a. global rather than localized EEG responses to stimuli. b. eye-movement problems that impair the ability to track objects. c. hypofrontality. d. a deficit in stimulus perception and cognitive processing.

Answer: c Textbook Reference: Etiology of Schizophrenia 10. All of the following evidence supports the idea that there is a strong genetic component to schizophrenia except

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a. the monozygotic twin concordance rate is 48% but they share 100% of their genes. b. first-degree relatives of schizophrenics are 12 times more likely than the general population to develop schizophrenia at some point in their lifetimes. c. second-degree relatives of schizophrenics are four times more likely than the general population to develop schizophrenia in their lifetimes. d. even when twins are reared apart, the difference in concordance rates is maintained, with the monozygotic rates always higher than the dizygotic rates.

Answer: a Textbook Reference: Etiology of Schizophrenia 11. Molecular genetic research a. has moved forward on the assumption that schizophrenia involves multiple genes located at different loci. b. has identified potential ―schizophrenia genes‖ on chromosomes 6, 8, 13, and 22. c. uses either linkage studies or considers candidate genes in its search for the genetic basis of schizophrenia. d. All of the above Answer: d Textbook Reference: Etiology of Schizophrenia 12. Which statement regarding the epigenetic modification of the RELN gene, which codes for the protein reelin, is false? a. Acetylation causes a more ―open‖ chromatin state and results in enhanced reelin production. b. Methionine makes schizophrenic symptoms worse for more than 60% of patients tested. c. Disruption of reelin production could affect neuronal positioning during development. d. Studies have demonstrated a decrease in reelin in the brains of schizophrenic patients that could be explained by hypermethylation.

Answer: a Textbook Reference: Etiology of Schizophrenia 13. The DISC1 gene codes for proteins and polymorphisms in this gene are associated with . a. involved in monoamine synthesis; impairments in working memory b. involved in intracellular transport and axon elongation; motor disturbances c. involved in neurogenesis and neuronal migration; impairments in performance on the WCST d. found in dendritic spines; enlarged ventricles Answer: c Textbook Reference: Etiology of Schizophrenia 14. Which of the following is not an example of a prenatal or perinatal complication that is associated with schizophrenia? a. Exposure to viral infection during the second trimester b. Being delivered by Caesarean section

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c. Oxygen deprivation during birth d. Severe malnutrition Answer: b Textbook Reference: Etiology of Schizophrenia 15. Which of the following does not support the idea that CNS stimulants produce a psychosis that strongly resembles schizophrenia? a. High doses of amphetamine in animals produce a syndrome of stereotyped licking, sniffing, and gnawing. b. Cocaine and amphetamine addicts often have hallucinations and delusions. c. Clinicians have difficulty discriminating between paranoid schizophrenia and druginduced psychosis. d. Amphetamine given to schizophrenics causes the occurrence of new symptoms.

Answer: d Textbook Reference: Preclinical Models of Schizophrenia 16. Prenatal inflammation models such as maternal exposure to polyI:C during pregnancy results in in hippocampal neurogenesis. a. short term increases b. long-term increases c. short-term decreases d. long-term decreases Answer: d Textbook Reference: Preclinical Models of Schizophrenia 17. Studies investigating the neonatal ventral hippocampal lesion model show that lesioned rats exhibit earlier and later in development, and that potentiates behavioral and biological outcomes. a. negative-like symptoms; positive-like symptoms; early stress b. negative-like symptoms; enhanced stress responses; tetrodotoxin c. positive-like symptoms; cognitive-like symptoms; antipsychotics d. enhanced stress responses; impaired cognitive function; antipsychotics Answer: a Textbook Reference: Preclinical Models of Schizophrenia 18. Which of the following does not support the dopamine hypothesis of schizophrenia? a. Amphetamine produces a greater release of dopamine in schizophrenics than in control subjects. b. Baseline levels of HVA do not differentiate controls and schizophrenics. c. Increased dopamine receptors are found in postmortem schizophrenic brains. d. Increasing the challenge dose of amphetamine makes schizophrenics’ positive symptoms get progressively worse.

Answer: b Textbook Reference: Neurochemical Models of Schizophrenia

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19. What model of schizophrenia integrates the neurochemical data with the neuroanatomical findings concerning the disorder? a. The dopamine hypothesis b. The glutamate-dopamine model c. The DA imbalance hypothesis d. The neurodevelopmental model Answer: d Textbook Reference: Neurochemical Models of Schizophrenia 20. Which of the following is not a part of the neurodevelopmental model of schizophrenia? a. Cognitive functions are most affected by the excess activity in the disinhibited mesolimbic pathway. b. Early damage to the mesocortical pathway results in the negative symptoms of schizophrenia. c. Hypofrontality results in a loss of inhibition of limbic structures, leading to positive symptoms. d. The developmental event that causes the initial damage could be one of many factors; it is not a specific causal agent.

Answer: a Textbook Reference: Neurochemical Models of Schizophrenia 21. What is evidence for a possible role for glutamate in schizophrenic symptoms? a. Overactivity of glutamatergic NMDA receptors can help explain the negative symptoms. b. Overactivity of glutamatergic NMDA receptors can help explain the cognitive symptoms. c. PCP or ketamine can worsen symptoms in individuals with schizophrenia. d. Increased levels of glutamate are found in postmortem studies of individuals with schizophrenia.

Answer: c Textbook Reference: Neurochemical Models of Schizophrenia 22. Which statement about the effectiveness of the traditional antipsychotic drugs is false? a. About one-third of patients respond very well to medications and may achieve a relatively normal life. b. Approximately one-third of patients remain hospitalized due to poor response to medication. c. The main therapeutic effect of these medications is to reduce cognitive deficits and emotional responsivity. d. About one-third of patients improve on medications but suffer relapses, and need a great deal of support and assistance to deal with daily stresses.

Answer: c Textbook Reference: Classic Neuroleptics and Atypical Antipsychotics

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23. All of the following evidence supports the idea that traditional antipsychotic medications act on the dopamine system except a. there is a decrease in dopamine-induced prolactin release from the pituitary gland during treatment with antipsychotic drugs. b. there is a positive correlation between the potency of an antipsychotic drug and its ability to displace a labeled ligand from dopamine receptors. c. antipsychotic drugs cause parkinsonian side effects, which are known to involve dopamine. d. antipsychotics that have lower affinity for DA receptors require higher doses to be clinically effective.

Answer: a Textbook Reference: Classic Neuroleptics and Atypical Antipsychotics 24. The receptor is most involved in the therapeutic effects of the traditional antipsychotics? a. D1 b. D2 c. D3 d. D4/5 Answer: b Textbook Reference: Classic Neuroleptics and Atypical Antipsychotics 25. The time course of effectiveness for antipsychotic medications has been explained by all of the following observations except that a. dopamine receptor blockade is not directly linked to clinical improvement. b. chronic dopamine autoreceptor blockade may result in receptor supersensitivity, and hence decreased dopamine turnover. c. depolarization block can occur in response to increased dopamine turnover, which results from the initial antipsychotic drug blockade of receptors. d. over time, antipsychotics decreased their binding to DA receptors and start acting at other receptor populations.

Answer: d Textbook Reference: Classic Neuroleptics and Atypical Antipsychotics 26. Which of the following is not a dopamine pathway affected by antipsychotic medications? a. Pathway from hypothalamus to pituitary b. Mesocortical pathway c. Pathway from the thalamus to the cortex d. Nigrostriatal pathway Answer: c Textbook Reference: Classic Neuroleptics and Atypical Antipsychotics 27. Parkinsonian symptoms in schizophrenia include all of the following except a. rigidity. b. sedation.

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c. akathesia. d. loss of facial expressions.

Answer: b Textbook Reference: Classic Neuroleptics and Atypical Antipsychotics 28. How can Parkinsonian side effects from antipsychotic medications be treated? a. Use anticholinergic drugs like Cogentin. b. Because these effects are due to receptor supersensitivity, add another dopamine blocker from the phenothiazine class. c. Use drugs that increase acetylcholine to balance the effects of dopamine blockade. d. Add an atypical antipsychotic to the traditional neuroleptic medications.

Answer: a Textbook Reference: Classic Neuroleptics and Atypical Antipsychotics 29. All of the following are true of tardive dyskinesia (TD) except a. it occurs in about 10–20% of people treated with neuroleptic medications. b. the cause of TD is not well understood, but it may be linked to excess dopamine receptors or a D1 -D2 receptor imbalance. c. the incidence of TD tends to decrease with increasing age of patients. d. it is a motor side effect of neuroleptics that may be irreversible in some patients.

Answer: c Textbook Reference: Classic Neuroleptics and Atypical Antipsychotics 30. Which of the following is not a neuroendocrine side effect of the traditional antipsychotic medications? a. Breast enlargement b. Lack of menstruation c. Inhibition of growth hormone d. Increased sex drive Answer: d Textbook Reference: Classic Neuroleptics and Atypical Antipsychotics 31. Doctors generally take into consideration all of the following side effects when choosing a particular antipsychotic drug for a schizophrenic patient except for a. sedation. b. autonomic side effects. c. hypotension. d. abuse potential.

Answer: d Textbook Reference: Classic Neuroleptics and Atypical Antipsychotics 32. Which statement about the abuse potential and dangers of antipsychotic medications is false? a. Antipsychotics are rarely abused because they produce no euphoria. b. Tolerance to the side effects of neuroleptics has not been observed, which helps to preserve their status as non-abused drugs.

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c. Neuroleptic medications have a high therapeutic index and are very unlikely to be involved in overdoses. d. Physical dependence and a withdrawal syndrome have not been observed with use of antipsychotic medications.

Answer: b Textbook Reference: Classic Neuroleptics and Atypical Antipsychotics 33. Why are selective D 2 receptor antagonists like sulpiride unacceptable as antipsychotic agents? a. They have common hormonal side effects. b. Their effects on the autonomic nervous system are not tolerated well by patients. c. They cause too much sedation. d. They impact the cardiovascular system more than researchers had hoped.

Answer: a Textbook Reference: Classic Neuroleptics and Atypical Antipsychotics 34. One of the newer types of atypical antipsychotic medications are a. phenothiazines. b. butyrophenones. c. dopamine system stabilizers. d. piperazines.

Answer: c Textbook Reference: Classic Neuroleptics and Atypical Antipsychotics 35. Abilify (aripiprazole) can simultaneously decrease DA receptor activation in some brain regions and increase it in others because it is classified as a(n) a. partial agonist. b. competitive antagonist. c. noncompetitive antagonist. d. inverse agonist.

Answer: a Textbook Reference: Classic Neuroleptics and Atypical Antipsychotics 36. Which statement regarding broad-spectrum antipsychotics is false? a. They block many receptor types, in addition to the D 2 receptor. b. They include the first discovered atypical neuroleptic, clozapine. c. They work best with some combination of D2 and 5-HT2 receptor blockade. d. They typically show high affinity for D 1 receptors.

Answer: d Textbook Reference: Classic Neuroleptics and Atypical Antipsychotics 37. All of the following are advantages of clozapine treatment of schizophrenia except a. it works more quickly than the older medications. b. it has a low incidence of motor side effects. c. it helps about 60% of patients who do not respond to traditional medications. d. it reduces negative symptoms of the disorder.

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Answer: a Textbook Reference: Classic Neuroleptics and Atypical Antipsychotics 38. Which of the following is not a drawback to using the drug clozapine to treat schizophrenia? a. It reduces the seizure threshold. b. It can cause agranulocytosis. c. It causes the dry mouth syndrome. d. It can cause cardiovascular problems.

Answer: c Textbook Reference: Classic Neuroleptics and Atypical Antipsychotics 39. Results from CATIE, a blinded controlled study comparing multiple antipsychotics to replicate ―real-world‖ prescriptions to a representative patient population, showed all of the following except that a. approximately 75% of patients had to switch medications. b. atypical drugs were no more effective than the classical neuroleptic. c. the newer drugs did a better job of reducing cognitive symptoms. d. the incidence of extrapyramidal symptom p s was the same for all drugs.

Answer: c Textbook Reference: Classic Neuroleptics and Atypical Antipsychotics 40. To address the cognitive symptoms of schizophrenia, new pharmacological approaches are being developed that target specific aspects of various neurotransmitter systems, including a. acetylcholine, dopamine, and glutamate. b. serotonin and glutamate. c. GABA and glutamate. d. glycine, dopamine, and GABA. Answer: a Textbook Reference: Classic Neuroleptics and Atypical Antipsychotics

Short Answer/Essay 41. Describe schizophrenia in terms of incidence, diagnosis, and symptoms. Distinguish between positive, negative and cognitive symptoms.

Answer: Approximately 1–1.5% of the population will suffer from schizophrenia. The symptoms are usually first observed in the late teens or early 20s, although it can also appear in childhood. Approximately 30% of people with schizophrenia will likely spend a significant proportion of their time in and out of hospitals and not respond well to treatment. Schizophrenia is often characterized by positive symptoms, often including dramatic symptoms such as delusions, hallucinations, and bizarre behavior. The negative symptoms are characterized by a decline or lack of normal behavior, including loss of motivation, social withdrawal, and anhedonia. These are harder to recognize. Finally,

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cognitive deficits can also be present in which working memory, attention, and executive function can be impaired.

Textbook Reference: Characteristics of Schizophrenia 42. How has schizophrenia been treated in the past? What happened in the 1950s to change this situation? Describe the typical course of schizophrenia, and indicate how patients are treated today.

Answer: Prior to the introduction of antipsychotics in the 1950s, patients with schizophrenia were typically hospitalized. With the introduction of the first antipsychotics, hyperactivity, manic symptoms, and positive symptoms disappeared for many people who were then released from the hospital. Possible outcome is often discussed in terms of the ―law of thirds‖: 1/3 of patients treated with antipsychotics show excellent response to the drug and may not ever need hospitalization even if they discontinue their medicine; 1/3 show improvement in symptoms but may experience relapse that requires hospitalization again from time to time; and 1/3 shows less recovery and may spend a considerable amount of time hospitalized.

Textbook Reference: Characteristics of Schizophrenia 43. Describe two structural and two functional abnormalities that have been reported in schizophrenia.

Answer: Many CT and MRI studies show cerebral atrophy and enlarged ventricles in individuals with schizophrenia. There are also a number of brain areas showing reduced volume including temporal lobes, prefrontal cortex, and several limbic regions. Temporal lobe and hippocampal differences tend to be the most consistent MRI findings. In terms of functional abnormalities, studies show a variety of effects, with the most consistent being reduced function of the prefrontal cortex (hypofrontality). There is also less cerebral blood flow while performing cognitive tasks that require PFC. Textbook Reference: Etiology of Schizophrenia 44. The genetic basis of schizophrenia has been explored by family studies, twin studies, linkage studies, searching for candidate genes, and using the microarray technique.

Describe evidence from three of these research areas.

Answer: In the general population, the incidence of schizophrenia is approximately 1%.

Both family studies and twin studies show that there is a significant genetic component for inheriting schizophrenia. First-degree relatives have an average lifetime risk 12 times higher (6–17%) than the general population. More distant (second-degree) relatives risk is still higher than the general population (average incidence of approximately 4% higher than the general population). Comparisons of monozygotic twins to dizygotic twins provide futher confirmation of the role of genetics. Dizygotic twins (that share the same proportion of genes as siblings but also share the same prenatal and usually postnatal environment) have a concordance rate of 17%. Identical twins (or monozygotic) who share virtually all of their genes in common have a 48% concordance rate. These studies provide a compelling argument for the role of genes, although there is also a role for environment, otherwise the concordance rate would be markedly higher. Linkage studies look for similarities in the loci in families with affected members and some of these have been identified as possible sites that increase the risk for developing schizophrenia.

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Textbook Reference: Etiology of Schizophrenia 45. Explain the current thinking on the biopsychosocial etiology of schizophrenia, including the early, latent, and late stages.

Answer: In this theory, genetic and environmental factors play an important role in the development of schizophrenia. As a developmental disorder, something happens during the early stage; this can be a genetic predisposition in combination with early environmental insults (exposure to viruses or toxins, birth complications, activated immune system, etc.). This is considered the first ―hit,‖ and is followed by the latent stage where early subtle signs begin to emerge (generally negative symptoms)— something occurring in adolescence when neurodevelopmental errors combine with environmental events to produce the symptoms that are components of schizophrenia (latent stage). The ―late stage‖ or ― second hit‖ typically occurs during adolescence when the neurodevelopmental errors can combine with adverse environmental events (i.e., stress, substance use, HPA disfunction) and can result in the symptoms that we recognize as schizophrenia.

Textbook Reference: Etiology of Schizophrenia 46. Describe two preclinical models of schizophrenia: amphetamine-induced stereotypy and the neonatal ventral hippocampal lesion (NVHL) model. Include a basic description of each model and evidence that supports their usefulness for understanding schizophrenia.

Answer: Amphetamine-induced stereotypy has been used as a classic screening device to identify effective antipsychotic drugs that block D 2 receptors. High doses of amphetamine can produce stereotyped sniffing, licking, and gnawing. Some researchers argue that this is similar to what is seen in humans and similar to the repetitions seen in schizophrenia. It does tend to mimic positive symptoms of schizophrenia but only in relation to DA, and so does not take into account other potential neurotransmitter involvement.

Textbook Reference: Preclinical Models of Schizophrenia 47. What is the prepulse inhibition of startle model and why is it used as an animal model for schizophrenia?

Answer: One model to explain schizophrenia focuses on their inability to screen out sensory stimuli and so they experience sensory overload because they are so overwhelmed by all of the sensory stimuli around them. The PPI model is a very reliable model to look at the ability to study sensory-filtering deficits. There are significant similarities in the paradigms used for testing humans and animal models which provide strength for the translation potential. The paradigm involves exposure to a weaker prestimulus (prepulse) and this subsequently inhibits the reaction of an organism to a subsequent strong startling stimulus (pulse). This reduced startle response is an indication that the subject cannot filter out unnecessary information (which some researchers argue is a significant issue for those with schizophrenia). In rodents, this can be induced by glutamate antagonists such as PCP, and then potential antipsychotic drugs can be tested for their ability to reverse these sensory-filtering deficits.

Textbook Reference: Preclinical Models of Schizophrenia

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48. Describe or diagram the neurodevelopmental model of schizophrenia.

Answer: This model integrates anatomical and neurochemical evidence to explain negative, cognitive, and positive symptoms based on altered DA function with the loss of specific nerve cell regions. This model suggests that the negative and cognitive symptoms are associated with reduced frontal lobe function. Evidence for this is that the negative and cognitive symptoms of schizophrenia share many of the same characteristics as those in patients with frontal lobe lesions. Furthermore, the severity of negative symptoms in individuals diagnosed with schizophrenia is correlated with reduced PFC metabolism, as measured by PET scans and reduced cerebral blood flow while doing a cognitive task. The second part of the model explains the positive symptoms of schizophrenia with evidence of hyperactive subcortical cells. The theory states that when inhibitory cortical feedback is lost, mesolimbic cells increase their activity. This model makes no attempt to identify the cause of the proposed early mesocortical cell loss.

Textbook Reference: Neurochemical Models of Schizophrenia 49. Describe the evidence linking glutamate abnormalities to schizophrenia, including findings from studies with PCP. What do these findings suggest for treatment possibilities?

Answer: It has been argued that glutamate hypofunction may play a role in the negative symptoms, the cognitive symptoms, and the impaired neural connectivity seen in schizophrenia. Some of the evidence for this: • Drugs that block glutamate NMDA receptors (such as PCP or ketamine) can produce psychotic symptoms that closely resemble schizophrenia (or exacerbates symptos in individuals with schizophrenia).

• A large genomic-wide association study identified 128 significant associations, many of which involve GLU function.

• Postmortem studies show decreased levels of GLU in PFC and hippocampus relative to controls.

• Some studies suggest that lower levels of the amino acid were correlated with greater brain atrophy.

Textbook Reference: Neurochemical Models of Schizophrenia 50. Cite evidence that shows that the traditional neuroleptics exert their clinical effects on the dopamine system, specifically dopamine receptors. Describe the homeostatic changes at the synapse that most likely account for the therapeutic effectiveness.

Answer: Drugs that have high affinity to D 2 receptors are effective at low concentrations, while drugs with low affinity for D 2 receptors need higher concentrations to be clinically effective. The clinical response to antipsychotic treatment is associated with an initial increase in dopamine (DA) metabolism, which is believed to reflect an increase in NT release. The increase in DA utilitization follows the acute blockade of autoreceptors on DA cells. The reason there is no worsening of symptoms is the drugs also block postsynaptic D 2 receptors. Chronic blockade with antipsychotics results in supersensitivity (up-regulation) of the autoreceptors. The up-regulation once again allows them to respond appropriately to DA by reducing DA synthesis, release, and metabolism.

Textbook Reference: Classic Neuroleptics and Atypical Antipsychotics

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51. List the four major dopamine pathways in the brain and identify the antipsychotic drug side effects associated with each. In general, how do doctors manage side effects when prescribing drugs for patients with schizophrenia?

Answer: The four major dopamine pathways are: • Mesolimbic pathway: projects from VTA to nucleus accumbens and other limbic areas. Involved in many behaviors and related to delusions and hallucinations of schizophrenia. DA antagonists reduce positive systems through this pathway.

• Mesocortical pathway: projects from VTA but sends axons to prefrontal and limbic cortex where it may have a role in the cognitive effects and negative symptoms of schizophrenia.

• Nigrostriatal pathway: begins in substantia nigra and projects to striatum.

Neuroleptic effects on this pathway are responsible for Parkinsonian tremor and perhaps other motor side effects.

• Tuberohypophyseal pathway: pathway from hypothalamus to pituitary gland that regulates pituitary hormone secretion. Blockade of DA receptors in this pathway contribute to a variety of neuroendocrine side effects.

Textbook Reference: Classic Neuroleptics and Atypical Antipsychotics 52. Describe the characteristics and possible neurochemical basis of one of the following serious side effects of neuroleptic medications: Parkinsonian symptoms or tardive dyskinesia.

Answer: Parkinsonian symptoms resemble Parkinson’s disease and can include tremors, akinesia (slowing or loss of voluntary movements), akathisia (restless discomfort in arms and legs, unable to sit still), loss of facial expression, and muscular rigidity. It is thought that drug-induced Parkinsonism is due to dopamine blockade in the same area of the brain that is responsible for Parkinson’s disease. DA receptor blockade in the striatum may result in a loss of inhibitory control of cholinergic cells and so there is excess ACh activity. To treat or reduce the likelihood of these side effects, one can prescribe anticholinergic drugs or use antipsychotics that inherently have anti-ACh effects, or use one of the newer atypical antipsychotics that has a lower than normal incidence of EPS. Tardive dyskinesia (TD) is also a motor side effect that is more often seen after prolonged use of antipsychotics. TD is characterized by stereotyped involuntary movements, typically of the face and jaw, and can include lip smacking, tongue protrusions, and sucking. There can also be uncontrolled movements of the trunks, limbs, and neck. It is most often seen in patients older than 60. The underlying neuropathology of TD is not known. For some patients the symptoms are irreversible; for others they can go away, although it often takes a long period of time, and this is far more likely to happen if people are younger.

Textbook Reference: Classic Neuroleptics and Atypical Antipsychotics 53. Explain how a dopamine receptor partial agonist can both reduce and increase DA activity, and indicate how this could be useful in the treatment of schizophrenia.

Answer: A drug such as aripiprazole is a DA partial agonist. Partial agonists will bind to DA receptors but produce less of an effect than DA itself. Thus, if there are overactive synapses (as there may be in schizophrenia), aripiprazole on board will reduce the effect

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of DA while the drug is on board, and reduce the positive symptoms. It also may increase DA activity in situations where there is too little DA activity and so may also be helpful in reducing negative symptoms.

Textbook Reference: Classic Neuroleptics and Atypical Antipsychotics 54. Explain why the atypical neuroleptics are referred to as broad -spectrum antipsychotics. Name the first drug in this category and identify its advantages and disadvantages over the older medications. Is it a perfect solutions for schizophrenia? Why or why not?

Answer: Broad-spectrum antipsychotics have this name because they block other receptor types in addition to D 2 receptors. Clozapine is an example of a broad-spectrum antipsychotic. It has relatively weak affinities for D 1 and D 2 and substantial serotonergic, muscarinic, and histaminergic affinities, as well as a high affinity for D 4 . There are a number of newer atypical neuroleptics that also bind with varying affinities to multiple neurotransmitter receptor subtypes. The advantages of clozapine and some of these newer antipsychotics is that they treat positive symptoms but they also may help treat negative symptoms. These atypicals often have a lower incidence of extrapyramidal motor side effects, as well as less endocrine side effects. They do have their own assortment of side effects, however, including a variety of metabolic side effects that can include significant weight gain, hyperglycemia, and elevated plasma cholesterol. There is often an increase in type 2 diabetes. Some of these second-generation drugs can also cause alterations in cardiac electrical activity. No drug is perfect and currently there is no single drug that works for everyone.

Textbook Reference: Classic Neuroleptics and Atypical Antipsychotics 55. Describe the research efforts currently underway to address the cognitive symptoms of schizophrenia, including work focused on dopamine, acetylcholine and glutamate.

Answer: There is considerable interest in drugs that can increase acetylcholine (ACh) activity (clozapine increases release of ACh and may improve cognitive function), and alternative drugs that act as positive allosteric modulators (PAMs) on one or more of the nicotinic receptors (α7 in particular) that enhance ACh activity. There is also interest in drugs that could act as D 1 agonists in the prefrontal cortex, either by specific D 1 agonist drugs or by reducing the breakdown of DA in the prefrontal cortex by drugs that inhibit the COMT enzyme (that breaks down DA in the synapse). Finally, there is interest in the possibility that enhancing glutamate activity could be another approach to improve cognitive function. While administering NMDA receptor agonists is not likely an option (since they increase neuronal hyperexcitability and risk for seizures), one approach that has been studied is using glycine site agonists that can enhance NMDA signaling as a coagonist.

Textbook Reference: Classic Neuroleptics and Atypical Antipsychotics

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Test Bank to accompany

Psychopharmacology, Third Edition Meyer • Quenzer

Chapter 20: Neurodegenerative Disorders Multiple Choice 1. The most significant risk factor for Parkinson’s disease is a. a history of boxing or other contact sports involving chronic skull impact. b. exposure to illicit drugs or environmental toxins. c. having family members with the disorder. d. age.

Answer: d Textbook Reference: Parkinson’s Disease 2. Two of the most frequent characteristics associated with Parkinson’s disease include and . a. difficulty initiating movement; slowness of movement b. unwanted motor activity; dementia c. pill-rolling tremors; retropulsion d. resting tremor; urge to move certain body parts Answer: a Textbook Reference: Parkinson’s Disease 3. Which motor dysfunction is not seen in Parkinson’s disease? a. Bradykinesia b. Pill-rolling tremor c. Rigidity d. Ballistic movements Answer: d Textbook Reference: Parkinson’s Disease 4. Although slowness of movement is a hallmark of Parkinson’s disease, some patients experience an uncontrollable acceleration of gait, called a. anteropulsion. b. akathisia. c. festination. d. dystonia.

Answer: c Textbook Reference: Parkinson’s Disease 5. Parkinson’s disease dementia affects approximately of disease progression.

of patients after 15 years

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a. 15% b. 15% to 40% c. 70% d. 100% Answer: c Textbook Reference: Parkinson’s Disease 6. Which of the following is the correct order of degeneration in Parkinson’s disease? a. Raphe nucleus and locus coeruleus → motor nucleus of the vagus → temporal mesocortex → temporal neocortex → substantia nigra b. Motor nucleus of the vagus → raphe nucleus and locus coeruleus → substantia nigra → temporal mesocortex → temporal neocortex c. Motor nucleus of the vagus → substantia nigra → raphe nucleus and locus coeruleus → temporal neocortex → temporal mesocortex d. None of the above; there is no typical order.

Answer: b Textbook Reference: Parkinson’s Disease 7. The major consequence of degeneration of substantia nigra cells is a decrease in input into the striatum, which results in less of the globus pallidus and greater tonic inhibition of the , reducing input to the cortex. a. NMDA; excitation; thalamus; excitatory b. dopamine; inhibition; subthalamic nucleus; inhibitory c. dopamine; inhibition; thalamus; excitatory d. acetylcholine; excitation; caudate/putamen; inhibitory Answer: c Textbook Reference: Parkinson’s Disease 8. Which statement about the ―MitoPark‖ mouse model is false? a. Substantia nigra cells die because of deficiencies in cellular respiration. b. Mice exhibit behavioral outcomes that resemble PD. c. MPP+ is transported into substantia nigra cells via the transporter. d. Treatment with L-DOPA reversed the observed behavioral changes.

Answer: a Textbook Reference: Parkinson’s Disease 9. Protein aggregation is an important component of neuronal degeneration in PD, with , composed of _ , formed in the affected cells. a. Lewy bodies; α-synuclein b. plaques; tau proteins c. neurofibrillary tangles; Lewy bodies d. proteosomes; ubiquitin Answer: a Textbook Reference: Parkinson’s Disease

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10. Pharmacological treatments for Parkinson’s disease include all of the following except drugs that a. prevent motor complications. b. prevent clinical progression of the disease. c. prevent the initial stages of neuronal degeneration. d. treat a particular symptom.

Answer: c Textbook Reference: Parkinson’s Disease 11. L-DOPA increases dopamine activity by , while the drug selegiline (Eldepryl) does so by . Pramipexole (Mirapex) does so by _. a. increasing synthesis; acting on DA receptors; inhibiting reuptake b. acting on DA receptors; inhibiting reuptake; inhibiting metabolism c. increasing DA cell firing; increasing synthesis; inhibiting reuptake d. increasing synthesis; inhibiting metabolism; acting on DA receptors Answer: d Textbook Reference: Parkinson’s Disease 12. Antipsychotic drugs are sometimes used for treating which symptom(s) in individuals with Parkinson’s disease? a. Resting tremor b. Difficulty initiating movement c. Hallucinations or delusions caused by DA agonists d. Depression Answer: c Textbook Reference: Parkinson’s Disease 13. Alzheimer’s disease is the most common form of dementia, affecting 25 million dementia patients worldwide. a. 25% b. 30 to 50% c. 50 to 70% d. 90% Answer: c Textbook Reference: Alzheimer’s Disease

of the

14. Which statement about mild cognitive impairment (MCI) is false? a. Consuming more than 2,100 calories a day increases the risk of MCI for people over age 70. b. MCI invariably leads to Alzheimer’s disease. c. People with MCI have trouble performing more than one task at a time. d. With MCI, difficult tasks take longer and longer to perform.

Answer: b Textbook Reference: Alzheimer’s Disease

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15. In addition to memory problems, a person afflicted with Alzheimer’s might exhibit all of the following except for a. difficulty driving. b. a lack of enjoyment of previously pleasurable activities. c. difficulty swallowing. d. impulse control issues and compulsive behaviors.

Answer: d Textbook Reference: Alzheimer’s Disease 16. Which of the following is not a psychiatric symptom seen in AD? a. Delusions b. Depressed mood c. Manic episodes d. Hallucinations Answer: c Textbook Reference: Alzheimer’s Disease 17. The primary cellular abnormalities in AD are and . These abnormalities are seen largely in cortex. a. amyloid precursor protein; beta-amyloid; prefrontal b. neurofibrillary tangles; amyloid plaques; frontotemporal association c. amyloid precursor protein; neurofibrillary tangles; frontoparietal association d. amyloid plaques; Aβ42; prefrontal Answer: b Textbook Reference: Alzheimer’s Disease 18. neurons are particularly susceptible to neurofibrillary tangles, which are primarily made of proteins. a. Pyramidal; tau b. Cholinergic; Aβ c. Prefrontal cortex; ubiquitin d. Polygonal; microtubule Answer: a Textbook Reference: Alzheimer’s Disease 19. The tau protein is normally associated with microtubules and is important in cellular function. In tangles, it is abnormally a. acetylated. b. folded. c. methylated. d. phosphorylated.

Answer: d Textbook Reference: Alzheimer’s Disease 20. The typical pattern of tangles in Alzheimer’s disease follows which pattern? a. Entorhinal cortex → hippocampus → neocortex

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b. Neocortex → entorhinal cortex → hippocampus c. Basal forebrain → entorhinal cortex → hippocampus → neocortex d. None of the above; degeneration occurs primarily in cholinergic and monoaminergic systems, not brain regions.

Answer: a Textbook Reference: Alzheimer’s Disease 21. The two most basic risk factors for AD are a. family history of dementia and advancing age. b. history of illicit substance use and advancing age. c. history of head trauma and bipolar disorder or PTSD. d. diabetes and high cholesterol.

Answer: a Textbook Reference: Alzheimer’s Disease 22. Familial cases of AD (known as autosomal dominant Alzheimer’s disease) are caused by mutations of genes, including , and make up of cases. a. risk; presenilin-1; 0.5% b. deterministic; apolipoprotein E; 5% c. deterministic; presenilin-2; 5% d. risk; apolipoprotein E; 15% Answer: c Textbook Reference: Alzheimer’s Disease 23. Which statement about apolipoprotein E is true? a. Its receptor may be increased in the brains of AD patients. b. The ApoE gene is a risk gene with only a minor influence on disease development. c. ApoE is normally involved in moving excess cholesterol from the blood to the liver. d. Early onset AD is not linked to the E4 form of the gene.

Answer: c Textbook Reference: Alzheimer’s Disease 24. Most patients develop plaques and tangles and some develop AD, possibly because they . a. heart disease; have high cholesterol b. Parkinson’s disease; develop Lewy bodies c. Huntington’s disease; carry the APP gene d. Down syndrome; have three copies of the APP gene Answer: d Textbook Reference: Alzheimer’s Disease 25. Which statement about the diagnosis of Alzheimer’s disease is false? a. It is a diagnosis of elimination. b. Amyvid can be used in conjunction with PET scans to tag beta-amyloid and confirm AD. c. Amyloid plaques can occur in individuals without AD.

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d. Other causes of dementia including stroke, vitamin deficiency, and chronic infection are ruled out before a diagnosis is made.

Answer: b Textbook Reference: Alzheimer’s Disease 26. A critical characteristic of a good animal model of AD is a. the development of neurofibrillary tangles. b. the presence of progressive neuropathology/symptomology. c. that it be naturally occurring. d. that it be in a mammalian species.

Answer: b Textbook Reference: Alzheimer’s Disease 27. Which statement about the cholesterol-fed rabbit model of AD is false? a. The rabbits only developed AD symptoms if they also were administered copper. b. The rabbits showed cognitive deficits, including impaired conditioning. c. Neurofibrillary tangles and αβ deposits were seen in the rabbits. d. Neuronal loss occurred in the frontal cortex and hippocampus.

Answer: a Textbook Reference: Alzheimer’s Disease 28. Multiple drugs that act as are currently in use for the treatment of AD. a. NMDA receptor agonists b. NMDA receptor antagonists c. cholinesterase inhibitors d. acetylcholine receptor agonists Answer: c Textbook Reference: Alzheimer’s Disease 29. Neurodegeneration leads to glutamate release and in the treatment of AD. a. depolarization block; an NMDA antagonist b. excitotoxicity; sodium channel blockers c. excitotoxicity; an NMDA antagonist d. excess neurotransmitter release; calcium channel blockers Answer: c Textbook Reference: Alzheimer’s Disease

, so

can be used

30. An increase in the levels of Bacteroidetes and reductions in two other bacteria (Firmicutes and Actinobacteria) have been implicated in a. Parkinson’s disease. b. Huntington’s disease. c. Alzheimer’s disease. d. ALS. Answer: c Textbook Reference: Alzheimer’s Disease

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31. The likelihood of developing Huntington’s disease depends on a. both inheriting the huntingtin gene and dietary factors. b. inheriting a huntingtin gene with more than 35 CAG repeats. c. both a family history of HD and advancing age. d. inheriting a huntingtin gene with more than 40 CAG repeats.

Answer: b Textbook Reference: Huntington’s Disease 32. Huntington’s disease is unusual compared to other neurodegenerative disorders in that a. it has both motor and cognitive symptoms. b. no cure exists. c. it has a clear genetic cause. d. HD patients may exhibit psychiatric symptoms.

Answer: c Textbook Reference: Huntington’s Disease 33. Which of the following is not a symptom of Huntington’s disease? a. Unwanted movements that cannot be suppressed b. Jerky, writhing movements of the limbs c. Problems swallowing d. Disturbances in the sense of touch and proprioception Answer: d Textbook Reference: Huntington’s Disease 34. Brains of HD patients show severe and . a. basal ganglia degeneration; enlarged lateral ventricles b. cerebellar degeneration; basal ganglia abnormalities c. enlargement of the lateral ventricles; degeneration of the prefrontal cortex d. striatal degeneration; enlarged fourth ventricle Answer: a Textbook Reference: Huntington’s Disease 35. The comorbidity of HD with psychiatric symptoms/disorders is problematic for treatment of HD symptoms. Decreasing excess movement is achieved therapeutically by or , but these treatments can lead to and . a. decreasing DA synthesis; blocking DA receptors; mania; dysphoria b. depleting vesicular DA; blocking DA receptors; depression; parkinsonism c. depleting vesicular DA; enhancing DA reuptake; schizophreniform symptoms; cognitive deficits d. increasing DA synthesis; increasing DA release; depression; mania Answer: b Textbook Reference: Huntington’s Disease 36. The early symptoms of amyotrophic lateral sclerosis (ALS) result from

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a. a loss of motor neurons. b. degeneration of muscle tissue. c. widespread destruction of the neuromuscular junction. d. degeneration of primary motor cortex.

Answer: a Textbook Reference: Amyotrophic Lateral Sclerosis 37. Which statement about ALS is false? a. Death is caused by respiratory failure as motor neurons controlling this process are lost. b. Protein aggregates known as spheroids are present in degenerating neurons. c. Abnormal eye movements may serve as a marker for the disease prior to other symptoms. d. Both hereditary and nonhereditary cases have been seen but genes have not been identified.

Answer: c Textbook Reference: Amyotrophic Lateral Sclerosis 38. Two very different approaches that are currently being used to treat ALS are and . a. DA agonists; GLU agonists b. GLU antagonists; free radical scavengers c. GLU agonists; free radical scavengers increasing neurotransmission in motor control centers of the brain d. DA antagonists; stem cell therapies to produce new motor neurons Answer: b Textbook Reference: Amyotrophic Lateral Sclerosis 39. Multiple sclerosis a. is thought to result from childhood vaccines. b. is easily diagnosed based on a core set of symptoms, including fatigue and problems with coordination. c. is thought to be a result from autoimmune destruction of the myelin sheath produced by oligodendroglia. d. may be accompanied by vision loss if the optic nerves are involved.

Answer: c Textbook Reference: Multiple Sclerosis 40. Which of the following is not considered a potential risk factor of MS? a. In utero exposure to the influenza virus b. Living in an extremely cold climate before age 15 c. Having a first-degree relative with MS d. Previous incidence of infectious disease, including mononucleosis Answer: a Textbook Reference: Multiple Sclerosis

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41. Treatments for MS include such as _ and treatments for exacerbations, such as . a. disease-modifying treatments; interferon beta; corticosteroids b. disease-modifying treatments; potassium channel blockers; corticosteroids c. treatments for managing symptoms; Copaxone; Augbagio d. treatments for managing symptoms; corticosteroids; interferon beta Answer: a Textbook Reference: Multiple Sclerosis 42. Treatment with a potassium channel blocker such as Ampyra could improve neurotransmission in demyelinated neurons because it a. enhances the generation of action potentials. b. allows transmission through demyelinated fibers in the motor pathway. c. hyperpolarizes the membrane. d. modulates release of acetylcholine at the neuromuscular junction.

Answer: b Textbook Reference: Multiple Sclerosis

Short Answer/Essay 43. Describe the factors that contribute to the ―Parkinson’s shuffle,‖ including information about rigidity and postural instability.

Answer: Rigidity or stiffness and inflexibility of joints are common symptoms of PD. This difficulty (together with bradykinesia) contributes to the Parkinson’s shuffle.

Textbook Reference: Parkinson’s Disease 44. Describe the stages of pathological changes in Parkinson’s disease and explain how a loss of dopaminergic cells in the substantia nigra leads to motor symptoms.

Answer: Braak stages suggest the following: Degeneration starts in dorsal motor nucleus of vagus and anterior olfactory structures. It then moves to raphe and locus coerulus. At stage 3 begins degeneration of neurons from substantia nigra, and this is when clinical diagnosis usually occurs because of the motor symtoms. Stages 4 and 5 (now combined) are degeneration of the temporal lobe mesocortex along with degeneration of sensory association and premotor areas of cortex. Finally, neocortex areas of primary sensory function and motor areas show degeneration in stage 6.

Textbook Reference: Parkinson’s Disease 45. Name the processes thought to be involved in neuronal degeneration in Parkinson’s disease.

Answer: Several processes contribute to the degeneration of neurons, including mitochondrial dysfunction, oxidative stress, inflammation, excitotoxicity, protein misfolding, and proteosomal dysfunction. These lead to Lewy body formation, other protein accumulation, and ultimately apoptosis of cells.

Textbook Reference: Parkinson’s Disease

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46. Explain why L-DOPA is the primary drug treatment for Parkinson’s disease. What is its mechanism of action? Identify three other ways DA receptor activation could be increased and name one drug from each of these categories.

Answer: L-DOPA is a metabolite in the synthesis of DA (the immediate preceding step).

L-DOPA is able to cross the blood–brain barrier which is why it is used. Other drugs used to increase dopamine signaling in the brain include monoamine oxidase inhibitors (MAOIs), catechol-O-methyltransferase inhibitors (COMT), and DA agonists. MAOIs prevent the breakdown of DA, NE, and EPI before they get repackaged into synaptic vesicles. COMT inhibitors also prevent the breakdown of DA in the synapse but are only given as adjuncts to L-DOPA. An example of an MOI is selegiline (Eldepryl); an example of a COMT inhibitor is entacapone; an example of a DA receptor agonist is ropinirole (Requip).

Textbook Reference: Parkinson’s Disease 47. Explain the process involved in the formation of amyloid plaques and neurofibrillary tangles and the consequences of their development. What is the normal function of beta-amyloid? Of tau protein?

Answer: Accumulation of beta amyloid (Aβ) protein between neurons in the brain results in the formation of amyloid plaques. Aβ is a protein fragment normally produced by the brain by enzymatic cleavage of amyloid precursor protein (APP). In healthy brain, there are several proposed functions of the fragments of APP including kinase activation, facilitation of gene transcription, cholesterol transport regulation, pro-inflammatory actions, and anti-microbial activities. Usually these fragments are degraded and cause no harm but in AD, the protein fragments (particularly Aβ42) accumulate to form the plaques. Neurofibrillary tangles are fibrous inclusions that are abnormally located in the cytoplasm of neurons. Tau protein is the primary component of the tangles. Tau is associated with microtubules that normally help maintain cellular structure and also participate in axonal transport. The tau in tangles is abnormally phosphorylated.

Textbook Reference: Alzheimer’s Disease 48. Describe animal models of AD in three different species. What are the advantages and disadvantages of each?

Answer: There are a number of transgenic mice that show the progressive neuropathology. These transgenic lines have mutations on the APP gene and produce memory deficits, high levels of Aβ42, and amyloid deposits. Aged beagles can develop learning and memory deficits as well as problems with executive function. This is a naturally occurring pathology similar to humans with cortical atrophy, lack of neurogenesis, β-amyloid plaques, etc. Cholesterol-fed rabbits developed Aβ deposits, neurofibrillary tangles, and cognitive deficits at a higher rate than controls, and if copper was added to the high cholesterol diet it was even worse.

Textbook Reference: Alzheimer’s Disease 49. Why might psychiatric disorders such as OCD and bipolar disorder be comorbid with Huntington’s disease? Consider the areas of neurodegeneration and the circuits that may be interrupted.

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Answer: HD patients often have difficulty with higher order functions. They have perseveration issues, learning and memory, and attentional problems. These effects are, in part, due to the connections from the basal ganglia to the dorsolateral prefrontal cortex, the orbitofrontal cortex, and the cingulate cortex. These regions play an important role in why we see the deficits we do in HD Textbook Reference: Huntington’s Disease 50. Explain why the nature of the disorder accounts for the fact that patients with ALS display primarily motor problems.

Answer: ALS is considered primarily a motor neuron disorder. Both upper and lower motor neurons degenerate, resulting in loss of fine and gross motor function.

Textbook Reference: Amyotrophic Lateral Sclerosis 51. Explain the procedures used to assess disease progression in MS and identify/describe the four courses the disease can take, including the incidence of each.

Answer: The four courses are: • Relapsing remitting MS: Occurs with the greatest frequency (85%) and is characterized by clearly defined attacks of neurological deficits, which are followed by times of partial or complete recovery. During remission, disease progression is halted.

• Primary progressive MS: Has a 10% frequency. Neurological deficits are experienced slowly but progressively worsen over time. Rate of progression varies. There can be periods of relapse and minor improvement (remissions) or plateaus.

• Secondary progressive MS: Approximately 50% of those with relapsing remitting MS developed this form before disease-modifying medications were available. LT data are not available on whether this number has declined. These patients start a period of steady decline. There may be periods of relapse and minor improvements or plateaus.

• Progressive/relapsing MS: This is about 5% and the worst case. Steady decline; clear attacks of worsening function. Some recovery but no periods of remission.

Textbook Reference: Multiple Sclerosis 52. What is meant by secondary or tertiary symptoms of MS? Include two examples.

Answer: The primary symptoms of MS can lead to secondary and tertiary symptoms of the disease. For example, if a person with MS has bladder dysfunction, they will have an increased risk for repeated urinary tract infections. Or prolonged periods of inactivity due to motor symptoms causing muscle weakness can result in pressure sores, decreased bone density, etc. Tertiary symptoms are those that are a result of the disease’s impact on a person’s life––loss of job, stress, failed relationships, social isolations, etc.

Textbook Reference: Multiple Sclerosis 53. Describe the different categories of treatments available for MS, give an example of each one and explain its mechanism of action.

Answer: Interferon beta-1a and -1b likely work in MS by increasing the function of suppressor T cells. These T cells modulate the immune system and so decrease the self-

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attack in MS. Examples include Avonex or Rebif. Copaxone (glatiramer acetate) is a synthetic protein that simulates myelin basic protein. It is thought to work by blocking myelin-damaging T cells. Novantrone (mitoxantrone), an antineoplastic agent, is a former cancer drug but is now available as an MS drug. This drug works because it suppresses several components of the immune system and thus reduces the self-attack by the immune system. Tysabri (natalizumab) is a monoclonal antibody that hampers movement of damaging immune cells from the bloodstream across the blood –brain barrier. Gilenya (fingolimod) is a sphingosine 1-phosphate receptor modulator. This causes retention of lymphocytes in lymph nodes, preventing their entry into the CNS through the blood – brain barrier, thus preventing inflammatory damage to neurons. Aubagio (teriflunomide) is a pyrimidine synthesis inhibitor that inhibits the function of specific immune cells.

Textbook Reference: Multiple Sclerosis 54. Many neurodegenerative disorders involve excess glutamate release from degenerating neurons. Why is this undesirable and how can the consequences be decreased?

Answer: In neurodegenerative diseases where neurons die, as the intracellular material is released into extracellular space, damaged/dying/dead neurons release significant amounts of glutamate that can cause excitotoxicity in nearby neurons. Administration of drugs that either block or modulate glutamate activity could reduce some of this secondary overexciation. Memantine, which is used for treating AD, is an example of a NMDA receptor antagonist, and uses this premise with the intent to prevent further excitotoxic neuronal damage.

Textbook Reference: Multiple Sclerosis

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