Psychopharmacology R.H. Ettinger Test BankPsychopharmacology RH Ettinger Test Bank

TEST BANK R.H. Ettinger Eastern Oregon University

Psychopharmacology 1/e

R.H. Ettinger Eastern Oregon University

CHAPTER 1 ORGANIZATION AND FUNCTION OF THE NERVOUS SYSTEM 1.1 Multiple Choice 1. The average human brain contains nearly ________ neurons. a. 10 billion b. 100 billion c. 200 billion d. 1 trillion Answer: C Diff: 1 Page Ref: 1 2. The three major classes of neurons are a. motor, sensory, and interneurons. b. efferent, afferent, and glia. c. motor, efferent, and afferent. d. glia, interneurons, and motor.

Answer: A Diff: 1 Page Ref: 1 3. The nucleus of a neuron resides within the a. terminal button. b. axon. c. cell body. d. dendrites.

Answer: C Diff: 1 Page Ref: 2 4. The axon hillock is located a. at a cell’s terminal button. b. at gaps in a cell’s myelin. c. where the axon leaves the cell body. d. where dendrites connect to the cell body.

Answer: C Diff: 1 Page Ref: 3 5. Myelin serves to a. increase the speed of conduction along the axon. b. insulate a cell’s axon from the electrical activity of adjacent axons. c. synthesize and store neurotransmitter substances. d. Both a and b are correct Answer: D Diff: 2 Page Ref: 3 6. Neurotransmitters are stored and released from a cell’s a. terminal button. b. node of Ranvier. c. cell body. d. axon hillock.

Answer: A Diff: 1 Page Ref: 3 3 .

7. The pressures acting on charged ions include ________ and ________ pressures. a. hydrostatic; electrostatic b. diffusion; hydrostatic c. diffusion; electrostatic d. diffusion; glucostatic Answer: C Diff: 2 Page Ref: 5 8. A neuron’s resting membrane potential is caused by a. sodium ions. b. a disequilibrium of positive and negatively charged ions inside and outside the axon. c. a high concentration of sodium inside the cell. d. potassium ions.

Answer: B Diff: 1 Page Ref: 5 9. The resting membrane potential has a charge of about ________ millivolts. a. 0 b. +100 c. –70 d. –55 Answer: C Diff: 1 Page Ref: 6 10. The resting membrane potential is maintained because a. potassium ions cannot cross through the cell membrane to the outside. b. sodium ions cannot cross to the inside of the cell membrane. c. there is no pressure acting on sodium ions. d. there is no pressure acting on potassium ions.

Answer: B Diff: 2 Page Ref: 7 11. Potassium is said to be at equilibrium during a resting potential because a. electrostatic pressure forcing it in equals the diffusion pressure forcing it out. b. diffusion pressure forcing it in equals the electrostatic pressure forcing it out. c. hydrostatic pressure forcing it in equals the electrostatic pressure forcing it out. d. it is equally concentrated inside and outside the cell.

Answer: A Diff: 2 Page Ref: 7 12. Changes in the voltage of a cell that vary depending on the strength of stimulation are referred to as a. action potentials. b. depolarization. c. hyperpolarization. d. graded potentials.

Answer: D Diff: 2 Page Ref: 7

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13. When an axon is depolarized to approximately ________ millivolts, an action potential is initiated. a. –55 b. –70 c. 0 d. +30 Answer: A Diff: 1 Page Ref: 7 14. Ion channels for sodium ions open when the membrane is ________ to about ________ millivolts. a. depolarized; –55 b. polarized; –70 c. charged; +30 d. depolarized; 0 Answer: A Diff: 1 Page Ref: 7 15. The initiation of an action potential is a consequence of an ________ of ________ ions. a. influx; potassium b. efflux; chlorine c. influx; sodium d. All of the above are correct Answer: C Diff: 1 Page Ref: 7 16. During an action potential, the membrane voltage changes from ________ to about ________ millivolts on the inside relative to the outside. a. –70; 0 b. 0; +50 c. –70; +30 d. –70; +55 Answer: C Diff: 1 Page Ref: 7 17. Local anesthetics such as lidocaine work by a. preventing the release of neurotransmitters signaling pain messages. b. blocking sodium channels so an action potential cannot occur. c. preventing cells from receiving signals from pain-transmitting neurons. d. blocking receptor sites for pain-signaling neurotransmitters.

Answer: B Diff: 2 Page Ref: 8 18. An action potential is initiated at a cell’s a. dendrites. b. axon hillock. c. terminal button. d. node of Ranvier.

Answer: B Diff: 1 Page Ref: 8

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19. Myelin is made up of ________ in the central nervous system. a. fat cells b. Schwann cells c. oligodendrocytes d. astrocytes Answer: B Diff: 3 Page Ref: 9 20. Myelin is made up of ________ in the peripheral nervous system. a. fat cells b. Schwann cells c. oligodendrocytes d. astrocytes Answer: B Diff: 3 Page Ref: 9 21. Gaps in myelin surrounding an axon are referred to as a. receptors. b. demyelination. c. nodes of Ranvier. d. synapses.

Answer: C Diff: 1 Page Ref: 9 22. The total amount of neurotransmitter released during an action potential depends on a. how much sodium enters the terminal button. b. how much calcium is ejected from the terminal button. c. regulatory proteins that contain the neurotransmitter substance. d. how much calcium enters the terminal button.

Answer: D Diff: 2 Page Ref: 11 23. Once released into the synaptic gap, neurotransmitter substances a. bind to receptor sites on both pre- and postsynaptic sites. b. are degraded by a breakdown enzyme. c. are returned to the transmitting cell via reuptake. d. All of the above are correct Answer: D Diff: 2 Page Ref: 12–13 24. Receptor proteins that directly control either the opening or closing of specific ion channels are referred to as ________ receptors. a. ionotropic b. metabotropic c. postsynaptic d. presynaptic Answer: B Diff: 2 Page Ref: 12

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25. Receptor proteins that indirectly open or close ion channels through the activation of a second messenger are referred to as ________ receptors. a. ionotropic b. metabotropic c. postsynaptic d. presynaptic Answer: B Diff: 2 Page Ref: 12 26. Which of the following is an example of a second messenger? a. Sodium b. A G protein c. Acetylcholine d. Cyclic adenosine monophosphate Answer: D Diff: 3 Page Ref: 12 27. Proteins on the presynaptic terminal that transport neurotransmitter substances back into the terminal button are referred to as a. G proteins. b. reuptake transporters. c. autoreceptors. d. metabotropic receptors.

Answer: B Diff: 2 Page Ref: 13 28. Receptors on the presynaptic terminal that regulate neurotransmitter synthesis and storage are referred to as a. heteroreceptors. b. autoreceptors. c. metabotropic receptors. d. Both a and b are correct Answer: D Diff: 2 Page Ref: 16–17 29. The main difference between autoreceptors and heteroreceptors is that a. heteroreceptors are activated by a different neuron and neurotransmitter, whereas autoreceptors are activated by the neuron they regulate. b. heteroreceptors are postsynaptic, whereas autoreceptors are presynaptic. c. heteroreceptors are metabotropic, whereas autoreceptors are ionotropic. d. heteroreceptors are excitatory, whereas autoreceptors are inhibitory.

Answer: A Diff: 3 Page Ref: 17

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30. Which of the following is NOT a criterion for a substance to meet the definition of a neurotransmitter? a. It must be synthesized and stored in the presynaptic neuron. b. It must cause a postsynaptic effect after it interacts with a receptor. c. It must be taken up intact by the transmitting neuron. d. It must have some mechanism for its degradation or reuptake.

Answer: C Diff: 2 Page Ref: 17 31. Otto Loewi received the Nobel Prize in 1936 for his discovery of ________. a. dopamine b. norepinephrine c. serotonin d. acetylcholine Answer: D Diff: 2 Page Ref: 19 32. The neurotransmitter that activates all neuromuscular synapses is called ________. a. norepinephrine b. acetylcholine c. dopamine d. muscarine Answer: B Diff: 2 Page Ref: 19 33. The neurotransmitter of the mesolimbic system is called ________. a. norepinephrine b. serotonin c. adenosine d. dopamine Answer: D Diff: 2 Page Ref: 23 34. The neurotransmitter involved in emotional behavior, arousal, and sleep that is derived from the amino acid tryptophan is called ________. a. dopamine b. norepinephrine c. serotonin d. acetylcholine Answer: C Diff: 3 Page Ref: 25 35. The most abundant excitatory neurotransmitter is called ________. a. GABA b. serotonin c. norepinephrine d. glutamate Answer: D Diff: 2 Page Ref: 26

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36. The glutamate receptor that has been implicated as a mechanism for long-term potentiation is called ________. a. NMDA b. metabotropic c. kainate d. AMPA Answer: A Diff: 2 Page Ref: 27 37. The most abundant inhibitory neurotransmitter is called ________. a. GABA b. serotonin c. Substance P d. glutamate Answer: A Diff: 2 Page Ref: 28 38. Alcohol binds to a specific receptor site on the ________ receptor complex. a. NMDA b. GABA c. dopamine d. norepinephrine Answer: B Diff: 3 Page Ref: 29 39. The neurotransmitter that transmits pain signals in the spinal cord is called ________. a. serotonin b. glycine c. Substance P d. nonrepinephrine Answer: C Diff: 2 Page Ref: 30 40. Anatomical sections through the brain along the axis from front to back are called ________ sections. a. coronal b. horizontal c. sagittal d. oblique Answer: C Diff: 2 Page Ref: 34 41. The respiratory center of the brain is located in the ________. a. medulla b. pons c. medbrain d. cerebellum Answer: A Diff: 3 Page Ref: 35

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42. Damage to the ________ might lead to jerky, uncoordinated movements. a. medulla b. pons c. medbrain d. cerebellum Answer: D Diff: 2 Page Ref: 37 43. A system of neurons originating deep in the brainstem which controls arousal, consciousness, and alertness is the ________ system. a. mesolimbic b. reticular activating c. striatal d. somatosensory Answer: B Diff: 2 Page Ref: 37 44. Which of the following structures is NOT part of the limbic system? a. Hippocampus b. Amygdala c. Medulla d. Nucleus accumbens Answer: C Diff: 3 Page Ref: 38 45. The mesolimbic-cortical system originates in the ________ and projects dopamine containing neurons to the ________. a. nucleus accumbens; frontal cortex b. septum; prefrontal cortex c. ventral tegmental area; frontal cortex d. ventral tegmental area; nucleus accumbens Answer: C Diff: 3 Page Ref: 39 46. The ________ undergoes considerable degeneration with prolonged periods of stress, schizophrenia, or post-traumatic stress disorder. a. hypothalamus b. hippocampus c. thalamus d. basal ganglia Answer: B Diff: 3 Page Ref: 39 47. The ventromedial nucleus, lateral nucleus, preoptic nucleus, and paraventricular nucleus are all parts of the a. hypothalamus. b. thalamus. c. basal ganglia. d. mesolimbic system.

Answer: A Diff: 2 Page Ref: 40 10 .

48. The ________ controls most sensory input to the cortex and is involved in regulating attention and arousal. a. hypothalamus b. basal ganglia c. medulla d. thalamus Answer: D Diff: 2 Page Ref: 41 49. Which of the following is NOT part of the basal ganglia? a. Caudate nucleus b. Putamen c. Substantia nigra d. Nucleus accumbens Answer: D Diff: 2 Page Ref: 41 50. Which of the following structures of the brain is affected by Parkinson’s disease? a. Thalamus b. Substantia nigra c. Nucleus accumbens d. Hippocampus Answer: B Diff: 2 Page Ref: 42 1.2 Discussion/Essay 1. Why does a neuron rest at –70 millivolts inside the cell membrane with respect to outside the cell membrane?

2. What are the differences between action potentials and graded potentials?

3. How does an action potential propagate along an unmyelinated axon?

4. How does myelin affect propagation? Why? 5. What happens to a neurotransmitter once it has been released?

6. What are receptors? What is their makeup?

7. What are the differences between ionotropic and metabotropic receptors?

8. What is a second messenger? Provide an example of one.

9. Describe the mechanisms for both EPSPs and IPSPs. 10. Describe the functions and differences between autoreceptors and heteroreceptors.

11. Review the following major neurotransmitters: ACh, NE, DA, SE, glutamate, GABA, and endorphins.

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CHAPTER 2 PSYCHOPHARMACOLOGY 2.1 Multiple Choice 1. Pharmacokinetics refers to the study of a. mechanisms of drug action. b. how drugs are developed and manufactured. c. drug administration, distribution, and fate. d. how drugs interact.

Answer: C Diff: 1 Page Ref: 44 2. N-methyl-3-phenyl-3[4-(trifluoromethyl)phenoxy]-propan-1-amine is an example of a drug’s ________ name. a. generic b. chemical c. brand d. trade Answer: B Diff: 2 Page Ref: 44 3. Prozac is an example of a drug’s ________ name. a. generic b. trade c. brand d. Both b and c are correct Answer: D Diff: 2 Page Ref: 45 4. The administration of hormones via skin patches is an example of ________ administration. a. subcutaneous b. transdermal c. intraperitoneal d. intramuscular Answer: B Diff: 1 Page Ref: 47 5. Which of the following methods is typically used to administer drugs for experimentation to small laboratory animals (e.g., mice and rats)? a. Intravenous b. Subcutaneous c. Inhalation d. Intraperitoneal Answer: D Diff: 1 Page Ref: 47

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6. The route of drug administration that results in the fastest peak plasma levels is ________. a. inhalation b. oral c. intravenous d. intranasal Answer: C Diff: 1 Page Ref: 48 7. The main advantage of administering drugs orally is a. it is relatively safe. b. its reliable absorption. c. it is easy to administer. d. All of the above are correct Answer: A Diff: 2 Page Ref: 48 8. Cell membranes are made up of phospholipid molecules arranged in a. two layers with their negatively charged heads forming the inner and outer surfaces. b. a single layer with their hydrophobic tails facing inward. c. two layers with their positively charged heads forming the inner and outer surfaces. d. two layers with their positively charged tails forming the inner and outer surfaces.

Answer: A Diff: 2 Page Ref: 49 9. Glucose and other larger substances are transported across cell membranes a. because of their fat solubility. b. because they are hydrophilic. c. by transporter protein molecules imbedded within the cell membrane. d. through gaps in the membrane surface.

Answer: C Diff: 2 Page Ref: 49 10. In order for a drug to pass through cell membranes, it must be a. water-soluble. b. lipid-soluble. c. hydrophobic. d. hydrophilic.

Answer: B Diff: 2 Page Ref: 49 11. The blood-brain barrier is constructed of a. tight junctions between astrocytic feet. b. an extra phospholipid layer in the cell membrane. c. negatively charged ions on the surface of the cell membrane. d. protein molecules imbedded in the cell membrane.

Answer: A Diff: 2 Page Ref: 50

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12. The blood-brain barrier a. is impermeable to all substances. b. is strongest in the area postrema of the medulla. c. prevents blood from leaving the brain. d. protects the brain from toxic substances, including most viruses and bacteria.

Answer: D Diff: 2 Page Ref: 51 13. The blood-brain barrier is weakest in which of the following areas of the brain? a. The subfornical area near the lateral ventricles b. The area postrema of the medulla c. The meninges surrounding the brain d. Both a and b are correct Answer: D Diff: 3 Page Ref: 51 14. When a drug binds to inactive sites throughout the body, this is referred to as a. metabolism. b. receptor binding. c. depot binding. d. distribution.

Answer: C Diff: 2 Page Ref: 51 15. A breathalyzer relies upon a. small amounts of alcohol being excreted through exhalation. b. small amounts of alcohol being excreted through perspiration. c. small amounts of alcohol remaining in the mouth after consumption. d. the detection of alcohol metabolites.

Answer: A Diff: 2 Page Ref: 51 16. A drug’s half-life is a. the amount of time it takes for a drug’s peak plasma level to be metabolized by 50 percent. b. the amount of time it takes for a drug’s initial blood level to be metabolized by 50 percent. c. one-half of a drug’s shelf life. d. the amount of time it takes for a drug to be equally distributed to tissues throughout the body.

Answer: B Diff: 2 Page Ref: 53 17. If a drug reaches tissue equilibrium one hour after administration and its plasma level decreases by one-half between hours 2 through 5 after administration, its half-life would be ________ hours. a. 5 b. 4 c. 3 d. 2 Answer: C Diff: 3 Page Ref: 53

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18. Which of the following statements is TRUE regarding the half-life of the antidepressant Prozac? a. It has a half-life of about two days. b. It has an active metabolite with a half-life of almost six days. c. Because of its relatively long half-life, missing a daily dose may not be problematic. d. All of the above are correct Answer: D Diff: 3 Page Ref: 53 19. A drug will have a longer duration of action if it a. has a short half-life. b. has a long half-life. c. has higher initial blood plasma levels. d. doesn’t have an active metabolite.

Answer: B Diff: 1 Page Ref: 53 20. Dose response curves are typically a. linear functions describing drug effects at different doses. b. “S”-shaped functions describing drug effects at different doses. c. “S”-shaped functions describing how a single dose affects different people. d. “S”-shaped functions describing how drug tolerance develops.

Answer: B Diff: 2 Page Ref: 54 21. Most drugs have a. a single dose response curve representing all of its effects at different doses. b. multiple dose response curves representing all of its effects at different doses. c. two dose response curves—one representing its initial effects and the other representing its effects after tolerance develops. d. a single dose response curve that can shift depending on how long the drug has been used.

Answer: B Diff: 3 Page Ref: 54 22. Drug tolerance can be defined as a a. decrease in a drug’s effectiveness after repeated administration. b. decrease in the rate of a drug’s metabolism. c. shift to the right in a drug’s dose response curve after repeated administration. d. Both a and c are correct Answer: D Diff: 3 Page Ref: 55 23. Cross-tolerance typically occurs when a. tolerance to a drug is rapidly lost. b. tolerance to a drug of one class, such as opiates, contributes to tolerance to a drug from a different class, such as barbiturates. c. metabolizing enzymes for a drug of one class begin to metabolize a drug from a different class. d. tolerance to a drug contributes to tolerance to a similarly acting drug.

Answer: D Diff: 2 Page Ref: 55

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24. Metabolic tolerance could develop as a consequence of a. Pavlovian conditioning to drug-associated cues. b. downregulation of receptor sites for a drug. c. an increase in the synthesis of metabolizing enzymes. d. a shift in the dose response curve.

Answer: C Diff: 2 Page Ref: 55 25. Cellular tolerance is typically a consequence of a. downregulation of receptors. b. an increase in the synthesis of metabolizing enzymes. c. Pavlovian conditioning of drug-associated cues. d. upregulation of receptor sites.

Answer: A Diff: 2 Page Ref: 56 26. If an animal expressed tolerance to a drug in one context but not in another, you would suspect this was an example of ________ tolerance. a. cellular b. metabolic c. behavioral d. associative Answer: D Diff: 2 Page Ref: 57 27. If after demonstrating associative tolerance to opiates in a specific context, you exposed an animal to the context repeatedly without the drug, you would see a. upregulation of receptors. b. downregulation of receptors. c. extinction of tolerance in that context. d. habituation of tolerance.

Answer: C Diff: 3 Page Ref: 57 28. The neural mechanism underlying associative tolerance is most likely a. habituation to the drug. b. cross-tolerance. c. downregulation of drug receptors. d. metabolic tolerance.

Answer: C Diff: 3 Page Ref: 57 29. Associative tolerance is a consequence of ________, whereas behavioral tolerance is a consequence of ________. a. operant conditioning; Pavlovian conditioning b. habituation; Pavlovian conditioning c. Pavlovian conditioning; habituation d. Pavlovian conditioning; operant conditioning Answer: D Diff: 2 Page Ref: 57

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30. If a laboratory animal is trained to perform a complex motor task under the influence of alcohol and later fails to perform the task without alcohol, this would demonstrate a. associative tolerance. b. cross-tolerance. c. state-dependent learning. d. upregulation.

Answer: C Diff: 2 Page Ref: 57, 59 31. The area of drug doses between a drug’s dose response curve for analgesia and its dose response curve for respiratory depression is called the a. LD50 dose b. LD100 dose c. therapeutic index d. placebo effect.

Answer: C Diff: 2 Page Ref: 59 32. When a patient responds positively to an inert substance, this is referred to as a. tolerance. b. upregulation. c. the placebo effect. d. the pseudo effect.

Answer: C Diff: 2 Page Ref: 60 33. Pharmacodynamics refers to the study of a. mechanisms of drug action. b. how drugs are developed and manufactured. c. drug administration, distribution, and fate. d. how drugs interact.

Answer: A Diff: 1 Page Ref: 62 34. Drugs that increase or facilitate neurotransmission are called a. antagonists. b. partial antagonists. c. psychoactive. d. agonists.

Answer: D Diff: 2 Page Ref: 62 35. Drugs that decrease or interfere with neurotransmission are called a. antagonists. b. partial agonists. c. inactive. d. agonists.

Answer: A Diff: 1 Page Ref: 62

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36. L-dopa, a drug used to treat Parkinson’s disease, is classified as an ________ because it ________. a. antagonist; disrupts dopamine release b. agonist; is a precursor for dopamine synthesis c. antagonist; blocks dopamine receptors d. None of the above are correct Answer: B Diff: 3 Page Ref: 63 37. A drug that blocks the reuptake of a neurotransmitter would be classified as a(n) a. agonist. b. antagonist. c. reuptake inhibitor. d. Both a and c are correct Answer: D Diff: 2 Page Ref: 63–64 38. The degrading enzyme for the neurotransmitters dopamine and nonrepinephrine is ________. a. MAO b. acteylcholinesterase c. acetyldehydrogenase d. acetylaldehyde Answer: B Diff: 2 Page Ref: 64 39. The drug Narcan (naloxone) is classified as an ________ because it ________. a. agonist; facilitates opiate binding to receptors b. antagonist; blocks opiate receptors c. antagonist; disrupts opiate synthesis and release d. Both b and c are correct Answer: B Diff: 3 Page Ref: 63 40. Botox is classified as an ________ because it ________. a. antagonist; inhibits the release of acetylcholine b. agonist; blocks the reuptake of acetylcholine c. agonist; blocks the degradation of acetylcholine d. Both b and c are correct Answer: A Diff: 3 Page Ref: 66 2.2 Discussion/Essay 1. Discuss why a drug needs to be lipid-soluble for it to have psychoactivity. Include in your discussion some details about membrane permeability and the blood-brain barrier.

2. Why do intravenous and inhalation administration methods result in getting a drug into the brain more quickly than oral or transdermal administration?

3. A drug that is lipid–soluble would be absorbed into all tissues and not just the brain. Does some of the drug absorbed by the peripheral tissues eventually get into the brain? If so, how?

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4. If a drug has a blood level at distribution equilibrium of 24 mg/L and a half-life of 4 hours, what would its blood level be after 12 hours?

5. Describe the following mechanisms of drug tolerance: metabolic, cellular, and associative.

6. Discuss the most likely candidates for the mechanism underlying associative tolerance.

7. Describe both antagonists and agonists as mechanisms of drug action. Select a drug in each category and provide details on its mechanism of action. (e.g., Amphetamine is a norepinephrine agonist. It increases NE release and reverses NE transporters.)

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CHAPTER 3 MOOD DISORDERS 3.1 Multiple Choice 1. The lifetime prevalence of major depression is estimated to be about ________ percent of the population. a. 30 b. 17 c. 50 d. 10 Answer: B Diff: 1 Page Ref: 69 2. All of the following are symptoms of major depression EXCEPT a. loss of appetite. b. dulled sense of pain. c. insomnia. d. motor agitation.

Answer: B Diff: 1 Page Ref: 70 3. 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 a significant life event such as the loss of a significant other or severe stress.

Answer: D Diff: 2 Page Ref: 71 4. Depression a. is often accompanied by agoraphobia. b. affects men and women equally. c. will not improve without therapy. d. has an average age of onset of 20 years.

Answer: A Diff: 2 Page Ref: 71 5. Monoamines are a. drugs used to treat depression. b. metabolites of major neurotransmitters. c. neurotransmitters that contain a single anime group in their molecular structure. d. drugs that can cause depression-like symptoms.

Answer: C Diff: 2 Page Ref: 71

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6. The earliest versions of the monoamine hypothesis could not a. distinguish which monoamine transmitters were involved in depression. b. determine the lag time between drug-induced changes in neurotransmitter availability. c. determine why depressed patients often have lower blood levels of BDNF. d. All of the above are correct Answer: A Diff: 2 Page Ref: 72 7. The observation that antidepressant treatment produces rapid changes in neurotransmitter availability but the symptoms of depression do not disappear as quickly is known as a. reactive depression. b. nonreactive depression. c. a lag time. d. downregulation.

Answer: C Diff: 3 Page Ref: 72 8. Neural structures that often show signs of degeneration in untreated depression include the ________ and ________. a. frontal cortex; hippocampus b. frontal cortex; thalamus c. hypothalamus; frontal cortex d. None of the above are correct Answer: A Diff: 2 Page Ref: 72 9. The monoamine hypothesis assumes that depression is a consequence of a. low levels of all neurotransmitters. b. neural degeneration caused by monoamine neurons failing to produce amounts of growth factors. c. downregulated receptor numbers. d. the overexpression of amine receptors.

Answer: B Diff: 2 Page Ref: 72 10. Brain-derived neurotropic factor (BDNF) is a. a toxin produced by the brain that contributes to cell loss. b. a nerve growth hormone produced by neurons. c. essential for normal cell survival and receptor growth. d. Both b and c are correct Answer: D Diff: 2 Page Ref: 72 11. The synthesis of BDNF depends on sufficient a. influx of Ca++ following neural activation. b. dietary amines. c. levels of precursors for serotonin. d. exposure to light.

Answer: A Diff: 3 Page Ref: 72

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12. Downregulation of monoamine neurons a. disrupts neuronal signaling and plasticity. b. occurs as a result of neuronal inhibition by autoreceptors. c. may lead to cellular degeneration. d. All of the above are correct Answer: D Diff: 2 Page Ref: 72 13. Long-term antidepressant treatment leads to a. tolerance and a return of symptoms. b. downregulation of amine receptors. c. a decreased number of autoreceptors for norepinephrine and serotonin. d. an increased number of autoreceptors for norepinephrine and serotonin.

Answer: C Diff: 3 Page Ref: 73 14. The stress hormone cortisol a. causes a depletion of amine neurotransmitters. b. leads to downregulation of amine receptors. c. increases CREB activity in the cell nucleus. d. contributes to BDNF downregulation.

Answer: D Diff: 2 Page Ref: 73 15. Animal studies of the effects of antidepressants have shown that they can a. decrease forced swim time. b. decrease lethargy and sleep time. c. suppress BDNF synthesis. d. Both a and c are correct Answer: D Diff: 2 Page Ref: 74 16. Which of the following is NOT primarily used for treating major depression? a. Selective serotonin reuptake inhibitors (SSRIs) b. Lithium therapy c. Monoamine oxidase inhibitors (MAOIs) d. Tricyclic antidepressants Answer: B Diff: 2 Page Ref: 75–79 17. Tricyclic antidepressants a. bind to the reuptake transporter proteins for both serotonin and norepinephrine. b. cause long-term adaptive changes at the synapse that are related to their therapeutic effects. c. increase levels of BDNF. d. All of the above are correct Answer: D Diff: 2 Page Ref: 76

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18. Which of the following statements is TRUE concerning the side effects of tricyclic antidepressants? a. Side effects are found in over 80 percent of people taking tricyclic antidepressants. b. If tricyclic antidepressants are taken with foods containing tyramine, increased norepinephrine storage and release may occur. c. Tricyclic antidepressants block histamine and acetylcholine receptors. d. The toxic effects of the tricyclic drugs are typically seen at doses exceeding 5 times their normal dose.

Answer: C Diff: 3 Page Ref: 76 19. Monoamine oxidase-A (MAO-A) deaminates all of the following monoamines EXCEPT a. dopamine. b. norepinephrine. c. serotonin. d. phenylanine.

Answer: D Diff: 3 Page Ref: 78 20. In 2003, the Food and Drug Administration (FDA) approved a newer selective MAOI called ________ for treating Parkinson’s disease. a. doxepin b. sertraline c. phenelzine d. selegiline Answer: D Diff: 1 Page Ref: 79 21. Which of the following side effects is a frequent reason for individuals terminating SSRI use? a. Anxiety b. Severe headaches c. Sexual dysfunction d. Muscle rigidity Answer: C Diff: 1 Page Ref: 80 22. A toxic reaction caused by excessive serotonin activity due to overmedication with SSRI antidepressants is called a. synaptic syndrome. b. serotonin syndrome. c. serotonin overdose. d. serotonin reactivity.

Answer: B Diff: 2 Page Ref: 80 23. The drop in prescriptions of SSRIs to adolescents after the FDA warned about suicide risk resulted in a. a decrease in adolescent suicides. b. an increase in adolescent suicides. c. no change in suicide rates for adolescents. d. an increase in the effectiveness of placebos for adolescents.

Answer: B Diff: 2 Page Ref: 82

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24. SNRI antidepressants a. work on different mechanisms underlying depression. b. are much more effective than SSRIs for most patients. c. inhibit the reuptake of both serotonin and norepinephrine. d. facilitate the reuptake of both serotonin and norepinephrine.

Answer: C Diff: 1 Page Ref: 83 25. The atypical antidepressant bupropion a. is also used to diminish cravings associated with smoking cessation. b. acts as a selective dopamine reuptake inhibitor. c. may be addictive because of its dopamine activity. d. Both a and b are correct Answer: D Diff: 2 Page Ref: 84 26. An active placebo differs from a traditional placebo in that it a. has some true therapeutic effects. b. is only given to experimental patients with their consent. c. causes similar side effects, such as dry mouth and drowsiness, as antidepressants do. d. actually improves most symptoms of depression.

Answer: C Diff: 1 Page Ref: 85 27. St. John’s Wort a. is as effective as an antidepressant for most patients. b. has the same mechanism of action as traditional antidepressants. c. inhibits the vesicular storage of monoamine neurotransmitters. d. All of the above are correct Answer: C Diff: 2 Page Ref: 88 28. Bipolar disorder differs from major depression in that patients must also experience a. numerous episodes of mania intermixed with depression. b. at least one episode of mania. c. psychotic features in addition to depression. d. depressive and manic symptoms simultaneously.

Answer: B Diff: 1 Page Ref: 90 29. Rapid-cycling bipolar disorder is characterized by ________ during a year. a. 10–12 episodes of depression b. 10–12 episodes of mania c. 4 or more episodes of depression or mania d. at least one episode of mania mixed with depression Answer: C Diff: 1 Page Ref: 90

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30. Genetic studies have concluded that a. several identified genes contribute to bipolar disorder. b. increased BDNF synthesis may predispose individuals to bipolar disorder. c. polymorphisms resulting in increased expression of the serotonin transporter gene strongly correlates with the incidence of major depression. d. None of the above are correct Answer: D Diff: 2 Page Ref: 93 31. Patients who have had untreated bipolar disorder for a long time are more likely to a. respond to medication. b. have evidence of neural degeneration and enlarged ventricles. c. express rapid-cycling symptoms. d. All of the above are correct Answer: B Diff: 2 Page Ref: 93–94 32. Antidepressants and mood-stabilizing drugs a. promote neurogenesis. b. cause significant weight gain. c. be cardiotoxic. d. diminish in effectiveness over time.

Answer: A Diff: 2 Page Ref: 94 33. ________ is credited with the discovery of lithium treatment for bipolar disorder. a. Sigmund Freud b. Solomon Snyder c. John Cade d. John Beck Answer: C Diff: 1 Page Ref: 94 34. Lithium acts by a. resolving a lithium deficiency in bipolar patients. b. deactivating a neurotoxin in the brains of bipolar patients. c. activating genes that code for the expression of serotonin transporters. d. increasing BDNF activity in the hippocampus and frontal cortex.

Answer: D Diff: 2 Page Ref: 96 35. The manic phases of bipolar disorder appear to be caused by a. a lithium deficiency. b. excessive dopamine activity. c. diminished serotonin activity. d. None of the above are correct Answer: B Diff: 2 Page Ref: 96

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3.2 Discussion/Essay 1. How are the symptoms of major depressive disorder both similar to and different from reactive depression?

2. What is BDNF? What is its role in normal neural functioning, and how is it altered in major depression?

3. How do antidepressants alter BDNF activity? Describe the evidence for this as well as the improvement in the symptoms of depression that occurs.

4. Why is it incorrect to state that SSRIs increase the “levels” of serotonin and that this is their mechanism of action?

5. How is bipolar disorder different from major depressive disorder?

6. How might the misdiagnosis and treatment of bipolar disorder as major depression increase the severity of the disorder?

7. Describe how mood stabilizers correct the underlying neurobiology of bipolar disorder.

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CHAPTER 4 ANXIETY DISORDERS 4.1 Multiple Choice 1. ________ is the most prevalent of all of the psychological disorders. a. Major depression b. Schizophrenia c. Anxiety d. ADHD Answer: C Diff: 1 Page Ref: 100 2. Fear and anxiety involve all of the following neural structures EXCEPT a. the amydgala. b. the hypothalamus. c. the thalamus. d. the basal ganglia.

Answer: D Diff: 2 Page Ref: 101 3. The amygdaloid nuclei are located a. in the brainstem. b. in the cerebellum. c. within the temporal lobes. d. posterior to the hypothalamus.

Answer: C Diff: 1 Page Ref: 101 4. The ________ and ________ control various fear responses such as the inability to move, facial expression, and heart and respiration rates. a. thalamus; amygdala b. medulla; hypothalamus c. pons; medulla d. orbitofrontal cortex; thalamus Answer: C Diff: 2 Page Ref: 101 5. The brain structure that sends inhibitory signals to the amygdala to diminish fear and anxiety is the a. thalamus. b. prefrontal cortex. c. hypothalamus. d. cingulate cortex.

Answer: B Diff: 2 Page Ref: 102

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6. Damage to the ________ diminishes one’s ability to respond appropriately in social contexts. a. amygdala b. thalamus c. prefrontal cortex d. cerebellum Answer: C Diff: 2 Page Ref: 102 7. The ________ receives sensory information about body states and during emotional responses. a. amygdala b. thalamus c. prefrontal cortex d. cingulate cortex Answer: D Diff: 2 Page Ref: 102–103 8. Damage to the cingulate cortex disrupts a. one’s ability to experience the subjective feeling of an emotion. b. the physiological state of an emotion. c. fear and anxiety responses (e.g., changes in heart rate, facial expression, etc.). d. facial expressions of all emotions.

Answer: A Diff: 2 Page Ref: 103 9. Anxiety differs from normal fear in that a. fear has an anatomical basis and anxiety does not. b. fear involves different neural structures than anxiety. c. anxiety is subjective, whereas fear is objective. d. anxiety can be experienced in the absence of an emotion-causing stimulus.

Answer: D Diff: 1 Page Ref: 103 10. Anxiety typically occurs when a. we are exposed to fear-producing stimuli and cannot withdraw from them. b. fear responses are not shut off after the stimulus is no longer present. c. we perceive an expectation of a vague threat or danger. d. All of the above are correct Answer: C Diff: 1 Page Ref: 103 11. Which of the following situations would normally cause anxiety as opposed to fear? a. An unfriendly dog rapidly approaching b. Preparing for an important exam c. Leaning over a high building d. Falling out of a raft in river rapids Answer: B Diff: 2 Page Ref: 103

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12. Which of the following is NOT one of the symptoms of a panic attack? a. Dizziness b. Parasesthesia c. Chest pain d. Dry mouth Answer: D Diff: 1 Page Ref: 104 13. The symptoms of trembling, accelerated heart rate, shortness of breath, chest pain, and dizziness are common with a. post-traumatic stress disorder. b. a panic attack. c. hysteria. d. a phobia.

Answer: B Diff: 1 Page Ref: 104 14. Which of the following disorders that often occurs after experiencing a severe accident, disaster, or horrific crime? a. Panic disorder b. Agoraphobia c. Post-traumatic stress disorder d. Generalized anxiety disorder Answer: C Diff: 1 Page Ref: 105 15. Stress can lead to a. GABA rebound and an excess of GABA activity. b. increased activity in the amygdala. c. decreases in volume in the hippocampus. d. Both b and c are correct Answer: D Diff: 2 Page Ref: 106 16. Functional neuroimaging studies have revealed ________ in the ________ in post-traumatic stress disorder patients. a. hypoactivity; amygdala b. hypoactivity; prefrontal cortex c. hyperactivity; prefrontal cortex d. hyperactivity; cingulate cortex Answer: B Diff: 2 Page Ref: 106 17. Functional neuroimaging studies have revealed ________ in the ________ in post-traumatic stress disorder patients following exposure to trauma-related stimuli. a. hyperactivity; amygdala b. hyperactivity; prefrontal cortex c. hypoactivity; cingulate cortex d. hyperactivity; cingulate cortex Answer: A Diff: 3 Page Ref: 106 29 .

18. The lifetime prevalence of generalized anxiety disorder is about ________ percent of the population. a. 10 b. 5 c. 2 d. 15 Answer: B Diff: 1 Page Ref: 108 19. Research has shown a strong association between the co-occurrences of ________ and ________. a. anxiety disorders; major depression b. post-traumatic stress disorder; early childhood experiences c. panic attacks; obsessive compulsive disorder d. excessive fear responses; anxiety Answer: A Diff: 1 Page Ref: 109 20. One way to investigate anxiety in laboratory animals (rats) is to measure their a. immobility in forced swim tasks. b. sleep and activity patterns. c. time in open arms of an elevated maze. d. blood levels of GABA. Answer: C Diff: 2 Page Ref: 109 21. Based upon our knowledge of the neural basis of fear and anxiety, the best class of drugs for treating anxiety disorders would be a. antidepressants (e.g., an SSRI). b. dopamine antagonists. c. GABA antagonists. d. GABA agonists.

Answer: D Diff: 3 Page Ref: 111 22. Drugs used to treat anxiety disorders were developed a. soon after the neurobiology of fear and anxiety were discovered. b. once the GABA receptor was identified. c. long before the discovery of GABA. d. from plant extracts with known anxiolytic properties.

Answer: C Diff: 2 Page Ref: 111 23. The first drugs developed to treat anxiety were derived from a. plant extracts with known anxiolytic properties. b. ethanol-containing products. c. barbituric acid. d. opium.

Answer: C Diff: 1 Page Ref: 111

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24. Which of the following statements best describes the GABAA receptor? a. It is a metabotropic receptor. b. It is an ionotropic receptor that controls the influx of Cl– ions. c. It is an ionotropic receptor that controls the influx of Na+ ions. d. It is still not well understood.

Answer: B Diff: 2 Page Ref: 113 25. When a barbiturate or alcohol receptor site is bound to a specific agonist, the neurotransmitter GABA a. does not bind to its receptor. b. binds to its receptor, but has no additional effect in the ion channel. c. increases the effectiveness and duration of GABA binding. d. is displaced.

Answer: C Diff: 3 Page Ref: 113 26. Postsynaptic membranes at GABAA synapses become ________ when GABA binds to its receptors. a. depolarized b. hyperpolarized c. unstable d. inhibited Answer: B Diff: 2 Page Ref: 113 27. The administration of diazepam-binding inhibitor (DBI) a. produces intense anxiety. b. causes sleep or sedation. c. produces a powerful calming effect. d. None of the above are correct Answer: A Diff: 2 Page Ref: 114 28. Barbiturates have all of the following effects EXCEPT a. sedation. b. respiratory depression at high doses. c. an increase in REM sleep. d. muscle relaxation.

Answer: C Diff: 2 Page Ref: 114 29. Benzodiazepines differ from barbiturates in that they a. bind to a different subunit on the GABAA receptor complex. b. do not produce sedation. c. do not open Cl– channels on their own. d. Both a and c are correct Answer: D Diff: 2 Page Ref: 116–117

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30. Which of the following statements regarding benzodiazepines is NOT true? a. All benzodiazepines agonize GABA neurotransmission by their activity on specific sites on the benzodiazepine receptor complex. b. The side effects of benzodiazepines are the same as alcohol intoxication. c. Benzodiazepines are rarely lethal by themselves in overdose. d. Benzodiazepines can cause physical dependence with long-term use and have great addictive potential.

Answer: D Diff: 2 Page Ref: 119 31. In addition to barbiturates and benzodiazepines, ________ are also used effectively to treat anxiety disorders. a. dopamine agonists b. serotonin agonists c. serotonin antagonists d. DBIs Answer: B Diff: 2 Page Ref: 119 32. ________ is a drug that has been abused for both muscle development by athletes and to facilitate rape. a. Flumazenil b. Gabapentin c. Rohypnol d. Gamma-hydroxybutric acid (GHB) Answer: D Diff: 2 Page Ref: 120 33. One herbal remedy known for its sedating and anxiolytic properties that has experimental support for its effectiveness in treating anxiety is a. St. John’s Wort. b. inositol. c. valerian root extract. d. None of the above are correct Answer: C Diff: 1 Page Ref: 121 34. The active, anxiety-reducing compounds in extracts of valerian root include a. ethanol. b. valernic acid. c. GABA. d. Both b and c are correct Answer: D Diff: 2 Page Ref: 123 35. The active compounds in valerian root extract appear to a. directly open Cl– channels at the GABAA receptor. b. increase GABA synthesis. c. bind to specific subunits on the GABAA receptor complex and facilitate GABA binding. d. be unknown at this time.

Answer: C Diff: 3 Page Ref: 124 32 .

36. Which of the following statements is TRUE regarding research on the effectiveness of inositol as an anxiety-reducing supplement? a. It is about as effective as benzodiazepines. b. It can reduce anxiety if combined with alcohol. c. It has been shown to reduce anxiety in experimental animals, but not in humans. d. That there is little evidence supporting its effectiveness.

Answer: D Diff: 1 Page Ref: 124 37. Obsessive compulsive disorder is characterized by a. episodes of depression mixed with anxiety. b. unwanted thoughts and repetitive behaviors. c. repeating thoughts and severe motor tics. d. depression and repetitive behavior.

Answer: B Diff: 1 Page Ref: 125 38. The underlying pathology of obsessive compulsive disorder appears to be a. dysfunctional circuitry between the orbitofrontal cortex, structures within the basal ganglia, and the cingulate gyrus. b. cellular degeneration of the orbitofrontal cortex. c. excessive activity of the prefrontal cortex and the cingulate gyrus. d. the absence of neural connections between the cingulate gyrus and orbitofrontal cortices.

Answer: A Diff: 3 Page Ref: 127 39. The most effective drug treatment for obsessive compulsive disorder are a. GABA agonists. b. dopamine antagonists. c. serotonin agonists. d. serotonin antagonists.

Answer: C Diff: 2 Page Ref: 130 40. A possible mechanism for drug treatment of obsessive compulsive disorder appears to be a. increasing dopamine receptors in the caudate nucleus. b. decreasing neural activity in the thalamus. c. decreasing activity in the cingulate gyrus. d. All of the above are correct Answer: D Diff: 2 Page Ref: 130 4.2 Discussion/Essay 1. Describe the role of the amygdala in fear and anxiety responses. Identify the structures within the amygdala as well as brain structures that receive input from them.

2. Which brain structures send signals to the amygdala to inhibit fear and anxiety responses? Which neurotransmitter is involved?

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3. Describe the differences and apparent functions of fear and anxiety.

4. What is the apparent pathology underlying post-traumatic stress disorder?

5. How might anxiety be investigated in experimental laboratory animals? What pharmacological evidence supports this methodology?

6. How might serotonergic neurons be involved in anxiety? Describe evidence which supports this.

7. Describe the common mechanism of action that most anxiolytic drugs have.

8. Discuss evidence from the text that herbal remedies may be as effective as benzodiazepines in the treatment of anxiety. What is their mechanism of action?

9. Describe the pathology suspected to underlie obsessive compulsive disorder.

10. What is a cingulotomy, and why would this be an effective treatment for severe obsessive compulsive disorder?

11. How is serotonin involved in obsessive compulsive disorder and its treatment?

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CHAPTER 5 PSYCHOTIC DISORDERS 5.1 Multiple Choice 1. Which of the following statements is TRUE regarding schizophrenia? a. Schizophrenia typically emerges in late childhood. b. The most distinctive features of schizophrenia is the presence of disorganized speech and behavior. c. Children of schizophrenic parents have a tenfold risk of developing the disease. d. The lifetime prevalence of schizophrenia worldwide is about 5 percent.

Answer: C Diff: 2 Page Ref: 132 2. Occasionally, the speech of a schizophrenic can be so disjointed that it is referred to as a. jumbled speech. b. word salad. c. speech derailment. d. None of the above are correct Answer: B Diff: 1 Page Ref: 133 3. Positive symptoms of schizophrenia are characterized by a. their likeliness to be eliminated with drug treatment. b. behavior that is not typically disruptive. c. excessive or distorted behavior. d. a lack of appropriate behaviors.

Answer: C Diff: 1 Page Ref: 134 4. Negative symptoms of schizophrenia are characterized by a. their unlikeliness to be eliminated with drug treatment. b. behavior that is not typically disruptive. c. excessive or distorted behavior. d. absent or deficient behavior.

Answer: D Diff: 1 Page Ref: 134 5. All of the following are negative schizophrenic symptoms EXCEPT a. muted expression. b. lack of speech. c. avolition. d. catatonic behavior.

Answer: D Diff: 1 Page Ref: 134 6. All of the following were treatments used for schizophrenia prior to the 1950s EXCEPT a. insulin shock. b. frontal lobotomy. c. physical restraint. d. phenothiazines.

Answer: D Diff: 1 Page Ref: 134 35 .

7. Antonio Moniz received the Nobel Prize in 1949 for his use of ________ as a treatment for schizophrenia. a. frontal lobotomy b. electric shock therapy c. chlorpromazine d. clozapine Answer: A Diff: 1 Page Ref: 134 8. The dopamine hypothesis of schizophrenia proposes that schizophrenia is a consequence of a. abnormally low dopamine activity. b. excessive dopamine receptors in certain brain regions. c. excessive dopamine activity in the striatum and mesolimbic pathways. d. excessive dopamine activity in the prefrontal cortex.

Answer: C Diff: 2 Page Ref: 135 9. An experimental procedure where amphetamines are administered to schizophrenic patients to measure dopamine release is called a. amphetamine sensitization. b. amphetamine challenge. c. receptor challenge. d. amphetamine psychosis.

Answer: B Diff: 1 Page Ref: 136 10. Which of the following statements is NOT true regarding evidence supporting the dopamine hypothesis? a. Amphetamine overdose appears similar to paranoid schizophrenia. b. Drugs that block dopamine receptors are effective in eliminating symptoms. c. Schizophrenic patients do not release dopamine after amphetamine administration. d. Schizophrenic patients tend to have more dopamine receptors than normal controls.

Answer: C Diff: 3 Page Ref: 136 11. According to the dopamine hypothesis, the negative symptoms of schizophrenia results from ________ activity in ________. a. hyperdopaminergic; the prefrontal cortex b. hypodopominergic; the mesolimbic system. c. hypodopominergic; mesocortical pathways to the prefrontal cortex d. None of the above are correct Answer: C Diff: 2 Page Ref: 136

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12. Evidence from neuroimaging studies suggests that schizophrenia is associated with a. global, rather than localized, EEG responses to stimuli. b. eye-movement problems that impair the ability to track objects. c. hypoactive prefrontal cortices. d. a deficit in stimulus perception and cognitive processing.

Answer: C Diff: 2 Page Ref: 136 13. Glutamate excitotoxicity is neuronal damage to cells as a consequence of a. excessive and prolonged glutamate activity. b. insufficient glutamate activity. c. hyperactivity of mesolimbic dopamine neurons. d. excessive GABA activity in the thalamus.

Answer: A Diff: 2 Page Ref: 138 14. Schizophrenic patients have depressed numbers of NMDA receptors in the ________ and the ________. a. thalamus; frontal cortex b. hippocampus; thalamus c. medulla; hippocampus d. frontal cortex; medulla Answer: B Diff: 2 Page Ref: 138 15. The antipsychotic effects of phenothiazines are mediated by their antagonism of ________ receptors. a. D1 b. D2 c. D3 d. D4 Answer: B Diff: 2 Page Ref: 140 16. It is estimated that the phenothiazine dose required to obtain a therapeutic effect must be sufficient to occupy between ________ and ________ percent of D2 receptors. a. 25; 35 b. 35; 45 c. 50; 60 d. 70; 80 Answer: D Diff: 2 Page Ref: 140 17. Phenothiazines a. can cause serious and often debilitating motor effects seen in Parkinson’s disease. b. include the medications risperidone and aripiprazole. c. are sometimes referred to as atypical antipsychotics. d. have fewer side effects than the new generation antipsychotics.

Answer: A Diff: 1 Page Ref: 140

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18. Extrapyramidal symptoms are debilitating motor disruptions that are a. caused in the pyramidal tracks descending from the medulla. b. not caused in the motor system itself. c. caused by damage to neurons above the pyramidal tracks. d. None of the above are correct Answer: C Diff: 2 Page Ref: 140 19. Long-term treatment with phenothiazines may cause a. severe memory deficits. b. sexual dysfunction. c. Parkinson’s disease. d. tardive dyskinesia.

Answer: D Diff: 2 Page Ref: 140 20. Tardive dyskinesia is characterized by a. facial tics. b. tongue extensions. c. rapid eye blinking. d. All of the above are correct Answer: D Diff: 1 Page Ref: 140 21. ________ was the first antipsychotic that appeared to improve the symptoms of schizophrenia without causing severe Parkinsonian-like effects. a. Haloperidol b. Chlorpromazine c. Risperidone d. Clozapine Answer: D Diff: 1 Page Ref: 141 22. New generation antipsychotic drugs, such as clozapine, do not cause severe motor dysfunction because they a. bind more tightly to D2 receptors. b. don’t block dopamine activity. c. are less competitive than dopamine in the basal ganglia. d. agonize serotonin more than dopamine.

Answer: C Diff: 2 Page Ref: 142 23. Which of the following is a serious side effect that can be caused by clozapine? a. Agranulocytosis b. Excessive oxidative stress to white blood cells c. Tardive dyskinesia d. Both a and b are correct Answer: D Diff: 1 Page Ref: 143

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24. Which of the following antipsychotics has NOT been approved by the FDA? a. Amisulpride b. Clozapine c. Risperidone d. Haloperidol Answer: A Diff: 1 Page Ref: 144 25. The most predictive feature of an antipsychotic’s propensity to cause extrapyramidal symptoms is a. how tightly it competes for D2 receptors in the basal ganglia. b. its affinity for serotonergic receptors. c. its affinity for cholinergic receptors. d. its antagonism of 5-HT2A receptors.

Answer: A Diff: 2 Page Ref: 145 26. It is alleged that glutamate dysfunction in the thalamus and hippocampus leads to ________ activity in the cortex and to the development of negative symptoms in later stages of schizophrenia. a. decreased BDNF b. excessive dopamine c. excitotoxic glutamate d. Both a and c are correct Answer: C Diff: 2 Page Ref: 145 27. Animals pretreated with ________ also demonstrate schizophrenia-like responses. a. dopamine antagonists b. amphetamines c. phenothiazines d. nicotine Answer: B Diff: 1 Page Ref: 146 28. An animal model of psychosis that has proven useful in investigating the effectiveness of antipsychotic drugs is a. prepulse inhibition. b. forced swimming. c. the elevated maze. d. None of the above are correct Answer: A Diff: 2 Page Ref: 146 29. ________ is an experimental procedure in which schizophrenics who have undergone drug treatment respond with a smaller startle response to a sudden noise that is preceded with a warning signal than untreated schizophrenics do. a. Sensitization b. Habituation c. Prepulse inhibition d. Reactive inhibition Answer: C Diff: 2 Page Ref: 146 39 .

30. About ________ to ________ percent of schizophrenic patients eventually respond to medication. a. 10; 15 b. 30; 45 c. 75; 85 d. 80; 100 Answer: C Diff: 2 Page Ref: 149 5.2 Discussion/Essay 1. Describe the differences between positive and negative symptoms of schizophrenia. Include in your discussion the underlying pathology of each.

2. Describe the dopamine hypothesis of schizophrenia. Include in your discussion evidence that supports it.

3. In light of what we know about glutamate excitotoxicity, discuss why it is important to diagnose and treat schizophrenia early.

4. Why might new generation antipsychotic drugs cause fewer extrapyramidal side effects than phenothiazines?

5. Why might animal models of schizophrenia (e.g., prepulse inhibition or amphetamine-induced schizophrenia) be useful in drug development and testing?

6. In addition to drug therapy, what other therapeutic interventions should be included in schizophrenia treatment?

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CHAPTER 6 ATTENTION AND DEVELOPMENTAL DISORDERS 6.1 Multiple Choice 1. ADHD is characterized by ________ and ________. a. excessive talking; an inability to follow instructions b. an inability to attend to tasks; an excessive display of motor activity and impulsivity c. inattention to cognitive tasks; excessive talking d. excessive fidgeting; disruptive classroom behaviors Answer: B Diff: 1 Page Ref: 150 2. Which of the following statements is TRUE regarding ADHD? a. A diagnosis of ADHD usually occurs in late childhood. b. In many cases, ADHD symptoms dissipate by early adulthood. c. Approximately 8 percent of children under age 10 is diagnosed with ADHD at any given time. d. Childhood ADHD frequently occurs with other behavioral disorders.

Answer: B Diff: 2 Page Ref: 151 3. All of the following behaviors would be consistent with an ADHD diagnosis EXCEPT a. trouble organizing activities. b. careless mistakes and inattention to detail. c. excessive speech. d. excessive concentration on a single task.

Answer: D Diff: 1 Page Ref: 152 4. The underlying pathology of ADHD involves a. cortical hypoarousal. b. reticular activating system abnormalities. c. depressed dopamine activity in the frontal cortices. d. All of the above are correct Answer: D Diff: 2 Page Ref: 152–155 5. Quantitative EEG studies of children affected by ADHD reveals a. hyperarousal of the cortex. b. hyperarousal of the motor systems. c. hypoarousal of most cortical areas. d. Both b and c are correct Answer: C Diff: 2 Page Ref: 152–153

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6. In normal individuals, the predominant EEG pattern during wakefulness is ________, whereas in individuals with ADHD it is ________. a. theta; beta b. beta; theta c. alpha; beta d. beta; delta Answer: B Diff: 1 Page Ref: 153 7. Cortical hypoarousal accounts for a. forgetfulness. b. excessive fidgeting. c. poor attentiveness and concentration. d. Both a and c are correct Answer: C Diff: 2 Page Ref: 153 8. Attentional regulation involves a. neural activation of appropriate sensory cortices. b. attending appropriately to specific sensory information. c. receiving sufficient sensory information from sensory receptors to activate sensory cortices. d. sufficient activation of the sensory thalamus.

Answer: B Diff: 1 Page Ref: 153–154 9. In individuals with ADHD, the thalamic reticular nucleus a. inhibits sensory information from activating the sensory cortex. b. is disinhibited. c. routes sensory information to the wrong sensory cortex. d. is not regulated by dopamine.

Answer: A Diff: 3 Page Ref: 154 10. The excessive activity observed in ADHD appears to be a. caused by hyperarousal of the motor systems. b. attempts by patients to self-stimulate an underaroused cortex. c. seizure-like excitability of motor areas of the cortex. d. unaffected by reinforcing or punishing contingencies.

Answer: B Diff: 2 Page Ref: 155 11. The dopamine-deficit theory of ADHD proposes that a. dopamine deficits in the mesolimbic system underlie ADHD. b. dopamine deficits in the cortex cause hypoarousal. c. dopamine deficits in the caudate nucleus and frontal cortex may contribute to cortical hypoarousal. d. ADHD is caused by dopamine deficiencies throughout the brain.

Answer: C Diff: 2 Page Ref: 155

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12. Evidence supporting the dopamine-deficit theory of ADHD includes finding a. an increased expression of dopamine transporters in the caudate nucleus. b. fewer dopamine transporters in the frontal cortex. c. decreased dopamine inhibitory control over arousal systems. d. depressed dopamine activity in the thalamic reticular nucleus.

Answer: A Diff: 3 Page Ref: 155 13. The most widely used assessment scale for measuring treatment outcomes for ADHD is the a. ADHD Rating Scale. b. Brown ADHD Scales. c. Ritvo-Freeman Real Life Rating Scale. d. Connor’s Global Index.

Answer: D Diff: 1 Page Ref: 156 14. A more objective assessment of ADHD that measures changes in cortical activity following treatment involves a. fMRI. b. Connor’s Global Index. c. EEG. d. Both a and c are correct Answer: D Diff: 1 Page Ref: 157 15. Which of the following was NOT a conclusion from the NIMH’s study of treatment options for ADHD? a. Drug abuse risk appears to decrease among stimulant-treated ADHD patients compared to their nontreated cohorts. b. Children treated with stimulant medication showed greater improvements in academic performance and social skills compared to children in the nonmedicated comparison groups. c. Intensive behavioral treatment was far superior to induced stimulant medication. d. Both a and b are correct Answer: C Diff: 3 Page Ref: 157 16. Amphetamines increase the availability of DA by a. increasing the release of NE and DA from synaptic vesicles. b. blocking the reuptake transporter of NE. c. causing the transporters for DA to act in reverse. d. All of the above are correct Answer: D Diff: 2 Page Ref: 158 17. Amphetamines cause a(n) ________ in cortical arousal by increasing ________. a. increase; cortical dopamine activity b. increase; NE activity in the reticular activating system c. decrease; dopamine activity d. Both a and b are correct Answer: D Diff: 1 Page Ref: 159–160 43 .

18. NE pathways originate in the ________ and project along the ________. a. locus coeruleus; reticular activating system b. raphe nucleus; reticular activating system c. locus coeruleus; cortical pathway d. reticular activating system; thalamus Answer: A Diff: 3 Page Ref: 160 19. Which of the following is a legitimate concern about using amphetamines to treat ADHD? a. Their addictive potential b. Patients selling them to others c. Tachycardia d. Weight gain Answer: C Diff: 2 Page Ref: 160 20. An amphetamine overdose a. rarely occurs. b. can cause chronic insomnia. c. can induce amphetamine psychosis. d. can cause Parkinson’s disease.

Answer: C Diff: 2 Page Ref: 160 21. ________ is the most widely prescribed drug for ADHD. a. Modafinil b. Methylphenidate c. Pemoline d. Atomoxetine Answer: B Diff: 1 Page Ref: 161 22. Which of the following statements best describes the drugs Ritalin and Strattera? a. They do not have similar mechanisms of action as amphetamines do. b. They block the reuptake of norepinephrine like amphetamines do. c. They only increase dopamine activity. d. They do not increase cortical arousal significantly.

Answer: B Diff: 2 Page Ref: 161 23. Modafinil increases ________ in the hypothalamus. a. NE activity b. histamine release c. DA activity d. orexin release Answer: D Diff: 2 Page Ref: 161

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24. Modafinal increases alertness in ADHD patients by a. increasing norepinephrine activity in the reticular activating system. b. inhibiting the thalamic reticular nucleus. c. increasing dopamine activity in the caudate nucleus. d. increasing histamine release in the tuberomammilary nucleus.

Answer: D Diff: 2 Page Ref: 161 25. The trade name for methylphenidate is ________. a. Strattera b. Modafinil c. Ritalin d. Dexadrine Answer: C Diff: 1 Page Ref: 162 26. Rett’s syndrome a. is the most common of all of the pervasive developmental disorders. b. is a less severe and more functional form of autism. c. occurs more frequently in males than females. d. occurs only in females.

Answer: D Diff: 2 Page Ref: 163 27. Asperger’s disorder is also known as a. early infantile autism. b. autistic psychopath. c. infantile schizophrenia. d. Rett’s syndrome.

Answer: B Diff: 2 Page Ref: 163 28. Which of the following symptoms is NOT consistent with a diagnosis of autism? a. Marked impairments in eye-to-eye contact, facial expression, and social behaviors b. Lack of, or a marked delay in, the development of spoken language c. Inflexibility in routines d. Motor tics in the face Answer: D Diff: 2 Page Ref: 163–164 29. A child inflicted with Asperger’s disorder has essentially the same symptoms as an autistic child EXCEPT a. restricted repetitive patterns of behavior. b. impairments in speech development. c. impairment in social interaction. d. Both b and c are correct Answer: B Diff: 1 Page Ref: 165

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30. Which of the following appears to be a major cause of autism? a. A decreased brain volume b. Underconnectivity of major intra- and interhemispheric regions of the brain c. An increase in the thickness of myelin in the corpus callosum d. None of the above are correct Answer: B Diff: 2 Page Ref: 167 31. Compared to normal control subjects, autistics demonstrate ________ activity in the ________ gyrus during sentence comprehension tasks. a. depressed; superior temporal b. increased; superior temporal c. less; inferior frontal d. Both b and c are correct Answer: D Diff: 2 Page Ref: 167 32. The ________ genu and ________ splenium are significantly smaller in people with autism. a. anterior; anterior b. posterior; posterior c. anterior; posterior d. posterior; anterior Answer: C Diff: 2 Page Ref: 169 33. The corpus callosum is a. a band of connecting neurons whose axons terminate in the cingulate gyrus. b. made up of cortical circuits that integrate intrahemispheric connections. c. a band of interconnecting mylelinated axons that unite cortical areas as well as intrahemispheric regions. d. essential for normal intelligence.

Answer: C Diff: 2 Page Ref: 169 34. There is a strong correlation between the size of the ________ and ________. a. genu; functional interconnectivity in the brain. b. splenium; the severity of ADHD. c. genu; the number of axons it contains. d. splenium; how well autistics respond to drug treatment.

Answer: A Diff: 2 Page Ref: 169 35. Autistic spectrum disorders commonly co-occur with symptoms of all of the following EXCEPT a. hallucinations. b. seizures. c. anxiety. d. hyperactivity.

Answer: A Diff: 1 Page Ref: 171

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6.2 Discussion/Essay 1. Discuss the diagnostic criteria that may help to distinguish between “normal” inattentiveness from an attention disorder.

2. Describe the underlying pathology of ADHD. How can this pathology be diagnosed?

3. What is the dopamine-deficit theory of ADHD, and what evidence supports this position?

4. How do amphetamines reverse the pathology of ADHD? Describe the mechanisms of action of amphetamines.

5. How do the mechanisms of action of modafinil differ from the mechanisms of action of amphetamines?

6. What is the theory of cortical underconnectivity of autism?

7. Discuss evidence that suggests that autism results from underconnectivity.

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CHAPTER 7 THE PHARMACOLOGY OF OPIATES AND ANALGESIA 7.1 Multiple Choice 1. The term morphine comes from the a. Hebrew word for bliss. b. Greek word for analgesia. c. Greek word for Morpheus, the god of dreams. d. term morph, which means to change or transform.

Answer: C Diff: 1 Page Ref: 172 2. In the mid-1800s, morphine quickly emerged as a a. cough suppressant. b. effective analgesic for surgical pain. c. treatment for fevers and diarrhea. d. All of the above are correct Answer: D Diff: 1 Page Ref: 172 3. The Harrison Narcotics Act was passed as an attempt to regulate a. the availability of morphine to convert into heroin. b. the manufacture and distribution of heroin. c. heroin’s availability to prescription only. d. which medical conditions morphine and heroin were to be used for.

Answer: B Diff: 1 Page Ref: 172 4. The illicit importation and distribution of heroin was largely curtailed by the a. Harrison Narcotics Act. b. Controlled Substances Act. c. Drug Enforcement Administration. d. None of the above are correct Answer: D Diff: 2 Page Ref: 172 5. Alkaloids are a. chemical compounds related to alkali metals. b. nitrogen-containing compounds produced by a variety of plants. c. compounds that all have the same molecular structure and effects on the brain. d. compounds that are synthesized from plant materials.

Answer: B Diff: 1 Page Ref: 174 6. Heroin is a. converted to morphine during its metabolism. b. less lipid-soluble than morphine. c. more potent than morphine if taken by mouth. d. None of the above are correct Answer: A Diff: 2 Page Ref: 174 48 .

7. Codeine is synthesized from ________. a. oxycodone b. thebaine c. morphine d. etorphine Answer: C Diff: 1 Page Ref: 175 8. Which of the following is the most potent derivative of opium? a. Morphine b. Heroin c. Oxycodone d. Etorphine Answer: C Diff: 1 Page Ref: 175 9. The structural difference between morphine and heroin is that heroin has a. no methyl groups. b. no acetyl groups. c. two acetyl groups. d. two methyl groups.

Answer: C Diff: 1 Page Ref: 176 10. Nociceptors detect a. intense pressure. b. extreme temperature. c. inflammation. d. All of the above are correct Answer: D Diff: 1 Page Ref: 176 11. “First” or early pain a. is transmitted by unmyelinated C fibers. b. provides information about the unpleasantness of the painful sensation. c. travels along myelinated Aδ fibers. d. is often accompanied by autonomic responses, such as nausea.

Answer: C Diff: 1 Page Ref: 176 12. The neurotransmitter released in the dorsal horn of the spinal cord by pain-signaling neurons is ________. a. acetylcholine b. substance P c. norepinephrine d. glutamate Answer: B Diff: 1 Page Ref: 176

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13. The ascending pain pathway beginning in the dorsal horn of the spinal cord is called the a. thalamic reticular system. b. nociceptive pathway. c. spinothalamic pathway. d. somatosensory pathway.

Answer: C Diff: 2 Page Ref: 176 14. The ascending pain pathway terminates in the a. thalamus. b. frontal cortex. c. limbic system. d. somatosensory and anterior cingulate cortices.

Answer: D Diff: 2 Page Ref: 176–177 15. The descending pain pathway originates in the a. periaqueductal gray area. b. thalamus. c. medulla. d. raphe nucleus.

Answer: A Diff: 2 Page Ref: 177 16. The descending pain pathway terminates in the a. raphe nucleus. b. cingulated cortex. c. medulla. d. Both a and c are correct Answer: D Diff: 2 Page Ref: 177 17. The most important descending pathways for modulation of spinal cord transmission of pain originate in the a. thalamus. b. pons. c. limbic system. d. anterior cingulate cortex.

Answer: B Diff: 2 Page Ref: 177 18. Opiate receptors are concentrated in the a. dorsal horn of the spinal cord. b. thalamus. c. raphe nucleus. d. Both a and c are correct Answer: D Diff: 2 Page Ref: 178

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19. The ________ receptor is presumed to be the most important of the opiate receptors for pain analgesia. a. mu b. kappa c. delta d. theta Answer: A Diff: 2 Page Ref: 179 20. Overdose death by opiates is mediated by a. cardiac complications. b. neural toxicity. c. respiratory depression. d. All of the above are correct Answer: C Diff: 1 Page Ref: 179 21. Dysphoria may be caused by antagonism of ________ receptors. a. kappa b. mu c. delta d. theta Answer: B Diff: 2 Page Ref: 179 22. Opiate receptors a. are metabotropic and control K+ efflux. b. are inhibitory. c. hyperpolarize postsynaptic membranes. d. All of the above are correct Answer: D Diff: 2 Page Ref: 180 23. Which of the following is an example of a pure agonist? a. Pentazocine b. Fentanyl c. Naltrexone d. Both b and c are correct Answer: B Diff: 1 Page Ref: 180 24. Partial agonists a. have more affinity for receptors than pure agonists. b. have both agonistic and antagonistic effects on receptors. c. have less affinity for receptors than pure agonists. d. are more useful clinically than pure agonists because they are not addictive.

Answer: C Diff: 1 Page Ref: 180

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25. Pure antagonists a. include drugs such as naloxone and naltrexone. b. can reverse the effects of a heroin overdose within minutes. c. have a high affinity for receptors, but do not exert any physiological effect on the receptor. d. All of the above are correct Answer: D Diff: 2 Page Ref: 180, 182 26. The reinforcing effects of opiates take place in the a. mesolimbic system. b. frontal cortex. c. cingulated cortex. d. amygdala.

Answer: A Diff: 2 Page Ref: 182 27. Increases in dopamine activity in the ________ mediate the reinforcing effects of opiates. a. striatum b. nucleus accumbens c. ventral tegmentum area d. cingulate cortex Answer: B Diff: 2 Page Ref: 182 28. A model of the neurobiology of opiate reinforcement suggests that opiates produce their effects by inhibiting ________. a. dopamine b. GABA c. dynorphin d. b-endorphin Answer: B Diff: 2 Page Ref: 182 29. Stimuli associated with ________ can control dopamine activity in the mesolimbic system. a. feeding b. engaging in sexual behavior c. social interaction d. Both a and b are correct Answer: D Diff: 2 Page Ref: 182 30. Tolerance to opiate drugs a. is primarily due to increased rate of metabolism. b. develops quickly. c. is largely mediated by Pavlovian drug onset cues. d. All of the above are correct Answer: D Diff: 1 Page Ref: 183–184

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31. The Centers for Disease Control estimates that there are approximately ________ opiate-dependent people in the United States. a. 10 million b. 1 million c. 500,000 d. 25,000 Answer: B Diff: 1 Page Ref: 185 32. The recidivism rate for first-time treatment for opiate abuse is about ________ percent. a. 25 b. 50 c. 80 d. 90 Answer: C Diff: 1 Page Ref: 186 33. Most opiate treatment programs utilize a. aversion therapy. b. synthetic opioids. c. methadone maintenance. d. a comprehensive residential treatment facility.

Answer: C Diff: 1 Page Ref: 186 34. When ________ is administered intravenously to opiate-dependent patients, withdrawals are experienced almost immediately. a. naloxone b. methadone c. antabuse d. None of the above are correct Answer: A Diff: 2 Page Ref: 186 35. Critics of methadone treatment for opiate abuse claim that it a. is not effective in reducing opiate dependency. b. is merely substitutes one addiction for another. c. it is more costly than a comprehensive residential treatment facility. d. Both a and b are correct Answer: D Diff: 3 Page Ref: 186 7.2 Discussion/Essay 1. What was the Harrison Narcotics Act? 2. Describe the principal opiate compounds that are derived from opium.

3. How does heroin differ from morphine? How does this affect its absorption?

4. What is the principal mechanism of action of opiates?

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5. Describe the major pain pathways and neural structures involved in pain perception and its analgesia.

6. Where do opiates work within the pain pathways to blunt pain messages?

7. How do opiates contribute to increased dopamine activity in the mesolimbic system?

8. What do self-administration experiments tell us about the abuse potential of drugs? Why might this animal model be useful in describing the addictive potential of drugs?

9. Describe the differences between metabolic, cellular, and associative tolerance. How could these be distinguished by experiment?

10. What does reinstatement imply for addiction recovery?

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CHAPTER 8 SUBSTANCE ABUSE AND THE NEUROBIOLOGY OF ADDICTION 8.1 Multiple Choice 1. The most recent national surveys on drug abuse estimate that the lifetime prevalence of substance abuse and dependency is approaching ________ percent of the U.S. population. a. 25 b. 15 c. 30 d. 10 Answer: B Diff: 1 Page Ref: 187 2. The number of individuals in the U.S. population who meet the criteria for substance abuse and dependency has a. dropped significantly over the past 10 years. b. increased significantly over the past 10 years. c. remained relatively stable over the past 10 years. d. increased because of new defining criteria.

Answer: C Diff: 1 Page Ref: 187 3. Alcohol addiction is more common in individuals who suffer from a. bipolar disorder. b. depression. c. anxiety disorders. d. All of the above are correct Answer: D Diff: 1 Page Ref: 189 4. Which of the following is NOT one of the DSM-IV-TR diagnostic criteria for substance dependence disorder? a. Tolerance to the substance b. A persistent desire to curtail substance use c. The appearance of the substance on a restricted drug list d. Use of the substance in spite of knowledge about problems associated with its use Answer: C Diff: 1 Page Ref: 190 5. The brain’s reward pathway most likely evolved a. as an unnecessary consequence of brain evolution. b. as a mechanism to ensure attention to significant stimuli, such as sexual partners and highly caloric foods. c. from more primitive structures that regulated hunger and thirst. d. Both b and c are correct Answer: B Diff: 2 Page Ref: 192

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6. The psychologists who originally identified structures within the reward pathway were ________ and ________. a. Skinner; Miller b. Thorndike; James c. Olds; Milner d. Hebb; Miller Answer: C Diff: 1 Page Ref: 192 7. The medial forebrain bundle is the bundle of axons projecting from the ________ to the ________. a. nucleus accumbens; cortex b. septum; substantia nigra c. ventral tegmentum area; nucleus accumbens d. hypothalamus; nucleus accumbens Answer: C Diff: 2 Page Ref: 192 8. The structures of the reward pathway comprise the ________ system. a. mesolimbic b. reticular activating c. striatal d. hypothalamic-septal Answer: A Diff: 1 Page Ref: 192 9. The major neurotransmitter of the reward system is ________. a. norepinephrine b. dopamine c. serotoinin d. acetylcholine Answer: B Diff: 1 Page Ref: 192 10. Which of the following is NOT a structure within the reward system? a. Septum b. Nucleus accumbens c. Medial forebrain bundle d. Hypothalamus Answer: D Diff: 2 Page Ref: 193 11. The mesocortical system originates in the ________ and projects to the ________. a. basal ganglia; hypothalamus b. medulla, thalamus c. ventral tegmental area; prefrontal cortex d. septum; striatum Answer: C Diff: 2 Page Ref: 193

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12. Cocaine and heroin produce greater euphoria when administered a. orally. b. in near lethal doses. c. intranasally. d. intravenously.

Answer: D Diff: 2 Page Ref: 194–195 13. The subjective euphoric effects of a drug a. predict its addictive potential. b. diminish with discontinued drug use. c. increase during abstinence. d. are not a reliable predictor of its abuse potential.

Answer: D Diff: 2 Page Ref: 196 14. The addictive potential of a drug may best be predicted by its a. euphoric effects. b. ability to maintain self-administration in animals. c. ability to directly increase dopamine activity. d. ability to induce both psychomotor and incentive sensitization.

Answer: D Diff: 2 Page Ref: 196 15. Incentive sensitization is a(n) a. conditioned change in a drug’s value. b. decrease in a drug’s ability to produce euphoria. c. increase in the incentive value of a drug. d. drug’s potential to increase motor activity.

Answer: C Diff: 2 Page Ref: 196 16. Which of the following is a consequence of incentive sensitization? a. A drug produces greater levels of euphoria. b. Drug-associated cues also gain incentive value. c. Tolerance develops more quickly. d. All of the above are correct Answer: D Diff: 2 Page Ref: 196 17. The ability of drugs to induce ________ appears to depend on neurological adaptations in mesolimbic areas resulting from rapid rates of drug administration. a. euphoria b. incentive sensitization c. psychomotor sensitization d. All of the above are correct Answer: D Diff: 2 Page Ref: 196

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18. As cellular activity in response to a drug increases, ________ is expressed in greater amounts. a. c-FOS protein b. cAMP c. PKA d. CREB protein Answer: A Diff: 3 Page Ref: 197 19. Which of the following neural adaptations occur as an addiction develops? a. Decreased c-FOS activity b. Deactivation of cAMP c. Increased CREB activity d. Both a and c are correct Answer: C Diff: 2 Page Ref: 197 20. The relationship between drug administration rate and c-FOS expression a. is undefined at this time. b. is a negative correlation. c. is a positive correlation. d. depends on drug dose.

Answer: C Diff: 3 Page Ref: 198 21. Which of the following statements is NOT true regarding drug addiction? a. A rapid rate of drug delivery and availability to the brain enhances CREB and c-FOS upregulation. b. Drug addiction is characterized by powerful and long-lasting behavioral changes that can be reinstated after long periods of abstinence. c. Drug addiction increases dopamine activity in the nucleus accumbens as well as in other structures of the mesolimbic pathway. d. Addicition occurs to a wide a range of drugs, all which have similar structural features.

Answer: D Diff: 2 Page Ref: 199 22. All known addictive drugs a. rapidly increase dopamine activity in the mesolimbic system. b. produce euphoria initially. c. maintain self-administration in animals. d. All of the above are correct Answer: A Diff: 1 Page Ref: 199 23. CREB and c-FOS proteins contribute to increased a. sensitivity to dopamine. b. numbers of D1 receptors. c. dendritic branching. d. All of the above are correct Answer: D Diff: 2 Page Ref: 199

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24. The treatment options available today for most drug addicts a. include both drug therapy and behavioral therapies. b. are largely unsuccessful. c. are expensive. d. Both a and b are correct Answer: D Diff: 2 Page Ref: 200 25. Active immunization against cocaine abuse involves the a. administration of a drug that competes with cocaine at receptor sites. b. stimulation of the production of actual antibodies against cocaine. c. administration of a drug that dampens the euphoric effects of cocaine. d. administration of drugs such as bupropion.

Answer: B Diff: 1 Page Ref: 200 26. Active immunization works by a. decreasing cravings for cocaine. b. blocking cocaine at receptor sites. c. attaching an antibody to the cocaine molecule, thus preventing it from crossing the blood-brain barrier. d. stimulating the breakdown of cocaine into inactive compounds.

Answer: C Diff: 2 Page Ref: 200 27. Laboratories have demonstrated effective immunization against the effects of ________ in laboratory animals. a. nicotine b. methamphetamine c. heroin d. All of the above are correct Answer: D Diff: 1 Page Ref: 201 28. Presently, there are a. several drugs on the market that can cure drug addiction. b. a number of successful behavioral treatments for drug addiction. c. no commercially available vaccines for addictive drugs. d. antibodies against all known addictive drugs.

Answer: D Diff: 2 Page Ref: 201 29. Which of the following is one of the reasons why drug treatment often fails? a. Drug-associated cues can themselves reinstate drug cravings after abstinence. b. There is no effective treatment for addiction. c. Addicts fail to comply with treatment program requirements during treatment. d. Addicts merely switch to a different drug.

Answer: A Diff: 2 Page Ref: 202

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30. Evidence has found that ________ and ________ are addictive. a. video game playing; sex b. gambling; sex c. video game playing; gambling d. None of the above are correct Answer: D Diff: 2 Page Ref: 205 8.2 Discussion/Essay 1. Explain why addiction implies a form of drug dependence, but dependence does not always imply an addiction. Provide an example of a drug to which we might become dependent upon, but not become addicted to.

2. Identify the neural structures and pathways of the mesolimbic system.

3. What is the drug self-administration procedure? Why is it useful in identifying potentially addictive substances?

4. Why are we confident that psychomotor and incentive sensitization predict a drug’s addictive potential?

5. What evidence supports the conclusion that rapid drug administration is critical for addiction?

6. Describe the specific neural adaptations that underlie drug addiction.

7. Describe the evidence which supports the potential for immunization against addictive substances (e.g., cocaine, heroin, nicotine).

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CHAPTER 9 THE PHARMACOLOGY OF SCHEDULED PSYCHOACTIVE DRUGS 9.1 Multiple Choice 1. Since 1999, there has been a very slight decline in all illicit drug use with the exception of a. alcohol. b. prescription pain medication. c. cocaine. d. tobacco.

Answer: B Diff: 2 Page Ref: 208–209 2. Which is the following is NOT classified as a Schedule II drug? a. Methamphetamine b. Cocaine c. Coedine d. Heroin Answer: D Diff: 1 Page Ref: 210 3. Cocaine was named by ________ after carefully describing its extraction and purification process. a. Albert Hofmann b. William Devane c. Albert Niemann d. Friedrich Gaedcke Answer: C Diff: 1 Page Ref: 212 4. Freud advocated the use of cocaine for ________. a. depression b. anxiety c. indigestion d. Both a and c are correct Answer: D Diff: 1 Page Ref: 212 5. The Harrison Narcotic Tax Act misclassified cocaine as a(n) ________. a. stimulant b. hallucinogen c. narcotic d. opiate Answer: C Diff: 1 Page Ref: 213 6. After the passage of the Harrison Narcotic Tax Act in 1914, a. cocaine was banned completely. b. the import of cocaine from South America dropped dramatically. c. the usage of cocaine by youths in the U.S. dropped by over 35 percent. d. cocaine was available only to licensed practitioners.

Answer: D Diff: 1 Page Ref: 213 61 .

7. Crack cocaine is synthesized from cocaine hydrochloride and a. baking soda. b. hydrochloric acid. c. benzolecgonine. d. sulphuric acid.

Answer: A Diff: 1 Page Ref: 213 8. The principle metabolites of cocaine are ________ and ________. a. ethyldehyde; cocaethylene b. benzoylecgonine; cocaethylemne c. benzoylecgonine; ecgonine d. cocaethylene; cocaacetate Answer: C Diff: 2 Page Ref: 215 9. When cocaine is used with alcohol, ________ is formed. a. benzoylecgonine b. cocaethylene c. ethylcocalene d. ecgonine Answer: B Diff: 2 Page Ref: 215 10. The subjective euphoric effects of cocaine are directly related to its a. dose. b. degree of DAT binding. c. rate of metabolism. d. blood level.

Answer: B Diff: 2 Page Ref: 215 11. Doses that typically induce euphoria in cocaine users occupy between ________ and ________ percent of DATs. a. 40; 50 b. 25; 35 c. 50; 75 d. 60; 80 Answer: D Diff: 1 Page Ref: 215 12. Cocaine acts by blocking the reuptake transporters for ________ on the presynaptic terminal. a. norepinephrine b. serotonin c. dopamine d. All of the above are correct Answer: D Diff: 1 Page Ref: 215

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13. The observation that DAT knockout mice retain cocaine’s reinforcing effects suggests that cocaine a. can also increase norepinephrine activity. b. increases serotonin activity in the ventral tegmental area. c. works differently on different species. d. that dopamine is not necessary for reinforcing effects of drugs.

Answer: B Diff: 3 Page Ref: 217 14. Cocaine’s effects on serotonin neurons, which regulate dopamine activity, occurs in the a. nucleus accumbens. b. caudate nucleus. c. frontal cortex. d. ventral tegmental area.

Answer: D Diff: 3 Page Ref: 217 15. Cocaine’s ability to ________ makes it ideal to use as an anesthetic for surgery. a. block pain signals in the brainstem b. dull pain c. constrict local blood flow d. Both b and c are correct Answer: D Diff: 3 Page Ref: 217 16. Cocaine’s anesthetic effects are produced by a. blocking dopamine reuptake. b. reversing the dopamine transporter. c. blocking sodium influx during an action potential. d. agonizing dopamine in the peripheral nervous system.

Answer: C Diff: 2 Page Ref: 218 17. Cocaine use is associated with a. myocardial infarction. b. cardiac arrhythmia. c. occasional sudden death. d. All of the above are correct Answer: D Diff: 1 Page Ref: 218 18. Cocaine’s anesthetic effects are mediated by ________ channel blockade. a. K+ b. Cl– c. Ca++ d. Na+ Answer: D Diff: 2 Page Ref: 218

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19. The chemical structure of amphetamines most closely resemble that of ________. a. norepinephrine b. serotonin c. dopamine d. GABA Answer: C Diff: 1 Page Ref: 219 20. Dexedrine was introduced in the early 1940s to treat a. attention disorders. b. narcolepsy. c. obesity. d. All of the above are correct Answer: D Diff: 2 Page Ref: 220 21. In the early 1970s, amphetamine production reached its all-time high of over ________ tablets. a. 10 million b. 100 million c. 1 billion d. 10 billion Answer: D Diff: 1 Page Ref: 220 22. Methamphetamine differs from amphetamine in that a. methamphetamine is more fat-soluble. b. amphetamine is more popular, but too expensive for users. c. amphetamine is synthetic, and methamphetamine is made from a natural substance. d. methamphetamine is smokable and amphetamine is not.

Answer: A Diff: 2 Page Ref: 221 23. Which of the following is a mechanism of action for amphetamines? a. It blocks the reuptake transporters for norepinephrine. b. It increases the amount of norepinephrine released into the synapse during neuronal firing. c. It reverses the reuptake transporter for dopamine. d. All of the above are correct Answer: D Diff: 2 Page Ref: 222 24. Users of MDMA report that it produces all of the following side effects EXCEPT a. increased self-perception. b. sedation. c. intimacy with others. d. teeth grinding.

Answer: B Diff: 1 Page Ref: 225–226

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25. MDMA has been demonstrated to ________ in squirrel monkeys. a. cause hallucinations. b. cause significant damage to cortical serotoninergic and dopaminergic neurons. c. be addictive d. All of the above are correct Answer: B Diff: 2 Page Ref: 226 26. MDMA exerts its agonistic effects primarily on ________ neurons. a. catecholamine b. serotonin c. norepinephrine d. cholinergic Answer: B Diff: 1 Page Ref: 226 27. MDMA is predominantly a ________ agonist. a. nonrepinephrine b. GABA c. serotonin d. dopamine Answer: C Diff: 2 Page Ref: 226 28. Synesthesia, often caused by LSD use, is described as a. a loss of sensory transduction. b. a form of localized anesthesia. c. the experience of one sensory modality (e.g., hearing) as another (e.g., vision). d. the blocking out of one sensory modality by overstimulation of another.

Answer: C Diff: 1 Page Ref: 227 29. Which of the following individuals is credited with the discovery of LSD? a. John Cade b. Solomon Snyder c. Albert Hofmann d. Jonathan Spencer Answer: C Diff: 1 Page Ref: 228 30. The psychotropic effects of LSD are approximately ________ times more potent than amphetamine or cocaine. a. 10 b. 100 c. 1,000 d. 10,000 Answer: C Diff: 1 Page Ref: 229

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31. Of all of the psychotropic drugs, only ________ has no confirmed overdose deaths associated with its use. a. cocaine b. amphetamine c. LSD d. nicotine Answer: C Diff: 1 Page Ref: 229 32. Psilocybin is derived from a a. fungus on rye. b. mushroom. c. cactus flower. d. morning glory flower.

Answer: B Diff: 1 Page Ref: 230 33. A recent review of the literature on LSD flashbacks concluded that they a. are unlikely to be genuine. b. can persist for years after LSD use. c. they are an uncommon occurrence with no known pathology. d. All of the above are correct Answer: C Diff: 2 Page Ref: 231 34. The hallucinogenic effects of LSD is mediated by a(n) a. increase in 5-HT2A activity in the brainstem. b. decrease in 5-HT activity in the cortex. c. increase in both NE and DA activity in the mesolimbic system. d. increase in glutamate activity in the auditory cortex.

Answer: A Diff: 2 Page Ref: 232 35. The hallucinogenic effects of psychedelics appear to be mediated by a. antagonism of cortical serotonergic neurons. b. agonism of serotonergic neurons in the somatosensory cortex. c. activation of the thalamo-cortical pathways. d. activation of the pontine reticular formation.

Answer: B Diff: 2 Page Ref: 232 36. The origins of marijuana are found in a. Europe. b. the Middle East. c. China. d. the United States.

Answer: C Diff: 1 Page Ref: 233

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37. CB2 receptors are located primarily a. on the presynaptic terminals of motor neurons. b. on the presynaptic terminals of hippocampal neurons. c. in lymphatic tissues of the immune system. d. in the basal ganglia.

Answer: C Diff: 3 Page Ref: 236 38. When activated, cannabinoid receptors a. inhibit cAMP formation and voltage-dependent Ca++ channels. b. agonize a metabotropic second-messenger system. c. cause an ionotropic chemical transmission. d. hypopolarize the cell.

Answer: A Diff: 3 Page Ref: 236 39. The endogenous cannabinoid that plays an important role in regulating neural activity that mediates memory formation, pain signaling, and reward is ________. a. anandamide b. 5-AG c. CP d. cannabis sativa Answer: A Diff: 1 Page Ref: 237 40. When compared to marijuana for medicinal purposes, Marinol has been found to a. be more effective. b. have a delayed onset. c. have more intoxicating effects. d. Both b and c are correct Answer: D Diff: 2 Page Ref: 237 41. Marijuana is used to treat glaucoma because THC a. decreases intraoccular pressure. b. increases blood flow to the retina. c. regulates pupil dilation. d. All of the above are correct Answer: A Diff: 2 Page Ref: 238 42. The use of marijuana a. irreversibly impairs learning. b. induces minimal detrimental effects on cognitive functioning. c. causes brain damage. d. is proven to facilitate aging and compromised immune functioning.

Answer: A Diff: 3 Page Ref: 236

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43. Animals administered high doses of THC exhibit symptoms characteristic of a. muscular dystrophy. b. Huntington’s disease. c. Parkinson’s disease. d. multiple sclerosis.

Answer: C Diff: 1 Page Ref: 239 44. Recent research on cannabinoids is focusing on how cannabinoids modulate motor neurons, which may be beneficial for patients with a. glaucoma. b. Parkinson’s disease. c. multiple sclerosis. d. Both b and c are correct Answer: D Diff: 1 Page Ref: 239 45. The antiemetic (antinausea) effects of marijuana are mediated by a. soothing irritation in the stomach lining. b. suppressing the gag reflex. c. decreasing activity in the cortical region regulating the vomiting reflex. d. directly inhibiting neurons in the area postrema that control vomiting.

Answer: D Diff: 2 Page Ref: 239 9.2 Discussion/Essay 1. Describe the five schedules for classifying drugs identified by the Controlled Substances Act. Provide examples of common drugs within each classification.

2. Describe the mechanisms of cocaine action as well as specific pathways involved.

3. What have experiments with DAT knockout mice confirmed about cocaine action? Describe the experiments and results.

4. Describe the use of cocaine as a local anesthetic.

5. Describe the mechanisms of amphetamine action.

6. Discuss the mechanisms of MDMA action.

7. How might one argue that MDMA is one of the most toxic of all of the recreational drugs?

8. Discuss why merely knowing the mechanisms of action for LSD and other psychedelic drugs seems to only provide a partial explanation for the profound effects these drugs produce.

9. Describe the mechanisms of action for marijuana. Include a description of the cannabinoid receptors and their functions.

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10. Prepare an argument either in support of or against the legalization of marijuana for medicinal purposes. This argument should be defended with reference to known effects of marijuana, not merely your personal opinion.

11. Discuss the experimental evidence both for and against an argument that marijuana can be addictive.

Be sure to review the definition of addiction as well as the characteristics of known addictive substances.

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CHAPTER 10 THE PHARMACOLOGY OF NONSCHEDULED PSYCHOACTIVE DRUGS 10.1 Multiple Choice 1. Approximately ________ percent of the population over 18 years of age has an alcohol abuse problem. a. 22 b. 15 c. 6 d. 10 Answer: C Diff: 1 Page Ref: 242 2. The term proof may have originated from a. tests by British sailors to determine the alcohol content of rum. b. the observation that a combination of rum and gunpowder ignited when the alcohol content was at least 50 percent. c. whiskey-making monks in Ireland during the early 1400s. d. Both a and b are correct Answer: D Diff: 1 Page Ref: 243 3. The legal limit for alcohol intoxication in most states is ________ percent. a. 0.04 b. 0.08 c. 0.10 d. 0.12 Answer: B Diff: 1 Page Ref: 244 4. A person is likely to lose consciousness if their blood alcohol concentration (BAC) is ________ percent or greater. a. 0.08 b. 0.15 c. 0.20 d. 0.30 Answer: D Diff: 2 Page Ref: 245 5. During its first phase of metabolism, alcohol is converted to ________ by the enzyme ________. a. alcohol dehydrogenase; aldehyde b. acetaldehyde; aldehyde dehydrogenase c. acetic acid; alcohol dehydrogenase d. None of the above are correct Answer: B Diff: 2 Page Ref: 246

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6. The drug ________ inhibits the aldehyde dehydrogenase metabolism of acetaldehyde and causes hangover symptoms. a. haloperidol (Haldol) b. disulfiram (Antabuse) c. tricyclic antidepressants d. naltrexone Answer: B Diff: 1 Page Ref: 246 7. Membrane fluidization refers to a. alcohol’s ability to disrupt membrane processes. b. excessive water inside the cell membrane. c. excessive alcohol inside of the cell. d. alcohol’s dehydrating effects on cells.

Answer: A Diff: 1 Page Ref: 247 8. Which of the following effects of alcohol does fluidization account for? a. euphoria b. analgesic effects c. reinforcement d. anxiolysis Answer: B Diff: 1 Page Ref: 247 9. Studies show that alcohol’s effects depend on a. increased GABA binding to its receptors. b. decreased dopamine activity in the mesolimbic system. c. the influx of Cl–. d. Both a and c are correct Answer: D Diff: 2 Page Ref: 248 10. Alcohol’s antagonism of NMDA receptors contributes to a. dizziness and loss of motor coordination. b. amnesiac effects on learning and memory. c. blackouts. d. Both b and c are correct Answer: D Diff: 3 Page Ref: 249 11. Which of the following statements is NOT true regarding alcohol and dopamine? a. GABAA receptor blockade in the ventral tegmental area results in increased mesolimbic dopamine activity. b. The effects of alcohol on mesolimbic dopamine release may be limited by neural inhibition in the ventral tegmental area. c. Alcohol ingestation at intoxicating doses increase dopamine release in the ventral tegmental area and basal ganglia. d. The mechanisms by which alcohol increases dopamine release remain unknown.

Answer: C Diff: 3 Page Ref: 250 71 .

12. Metabolic tolerance occurs as the liver produces compensatory increases in ________ and ________. a. P450; acetaldehyde b. NAD; ethanol c. aldehyde dehydrogenase; P450 d. alcohol dehydrogenase; P450 Answer: D Diff: 2 Page Ref: 251 13. Animals that learn a complex motor task under the influence of alcohol tend to perform better after training if they are a. tested on the same apparatus. b. also under the influence of alcohol. c. not under the influence of alcohol. d. allowed to recover from intoxication.

Answer: B Diff: 1 Page Ref: 251–252 14. Another term for ________ tolerance is state-dependent learning. a. associative b. cellular c. behavioral d. metabolic Answer: C Diff: 1 Page Ref: 252 15. The drug of preference in treating symptoms associated with alcohol withdrawal is a. an SSRI antidepressant. b. an antipsychotic. c. a benzodiazepine. d. disulfiram Answer: C Diff: 2 Page Ref: 253 16. There are approximately ________ million smokers in the United States. a. 29 b. 46 c. 35 d. 53 Answer: B Diff: 1 Page Ref: 255 17. Most nicotine is metabolized by ________ during first-pass metabolism. a. CYP2A6 b. aldehyde oxidose c. nAChR d. Both a and b are correct Answer: D Diff: 2 Page Ref: 256

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18. Presynaptic nicotinic acetylcholine receptors a. cause hyperpolarization when activated. b. decrease the amount of neurotransmitter released. c. increase the amount of neurotransmitter released. d. Both a and b are correct Answer: C Diff: 2 Page Ref: 257 19. In the peripheral nervous system, nAChRs are found in a. the hippocampus. b. neuromuscular junctions of voluntary muscles. c. cerebral cortex. d. locus coeruleus.

Answer: B Diff: 2 Page Ref: 258 20. Nicotine and other cholinergic drugs have been used to treat a. Parkinson’s disease. b. arthritis. c. multiple sclerosis. d. Alzheimer’s disease.

Answer: D Diff: 1 Page Ref: 258 21. Acute nicotine tolerance appears to result from a. long-term exposure to nicotine products. b. rapid internalization of nicotinic acetylcholine receptors. c. rapid desensitization of nicotine acetylcholine receptors and the closing of cation channels. d. None of the above are correct Answer: C Diff: 3 Page Ref: 259 22. Nicotine’s behavioral sensitization may be mediated by a. downregulation of nicotinic acetylcholine receptors in the cortex. b. downregulation of dopamine receptors in the nucleus accumbens. c. upregulation of nicotinic acetylcholine receptors in the ventral tegmental area. d. Both b and c are correct Answer: C Diff: 3 Page Ref: 261 23. The structural changes to the nicotinic α4β2 receptor that appear to underlie nicotine dependence a. takes years to occur. b. can occur after smoking one or two cigarettes. c. only occurs in those with a genetic predisposition for these changes. d. is reversed quickly after smoking cessation.

Answer: B Diff: 2 Page Ref: 262

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24. Which of the following treatments for smoking cessation has NOT been investigated in humans, but seems to work in animals? a. Zyban b. Chantix c. Nicotine immunization d. None of the above are correct Answer: C Diff: 2 Page Ref: 264 25. A major difference between immunotherapy for nicotine dependence and drug treatment for nicotine withdrawal is that immunization a. only prevents the drug from entering the brain. b. releases dopamine receptors in the frontal cortex. c. alone precipitates withdrawal symptoms. d. Both a and c are correct Answer: D Diff: 3 Page Ref: 265 26. After caffeine is absorbed, it is a. metabolized in the liver by P450. b. distributed to the brain. c. metabolized into cotinine. d. None of the above are correct Answer: B Diff: 2 Page Ref: 268 27. Caffeine relieves headache pain by a. constricting cerebral blood vessels. b. releasing endorphins. c. blocking the release of substance P. d. decreasing blood pressure.

Answer: A Diff: 1 Page Ref: 267–268 28. Caffeine is considered an ergogenic drug because it a. decreases fatigue. b. increases metabolism. c. increases cardiac contractility and oxygen utilization. d. increases muscle contractility and force.

Answer: C Diff: 1 Page Ref: 268 29. Which of the following best describes caffeine’s effects on people suffering from anxiety? a. It serves as an inhibitor and reduces anxiety. b. It increases anxiety. c. It has little or no effect. d. It is therapeutic, but only when combined with other stimulants.

Answer: B Diff: 1 Page Ref: 268

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30. Caffeinism is a. severe withdrawals associated with disuse of caffeine. b. nausea and vomiting associated with caffeine overdose. c. an increase in heart and respiratory rates associated with caffeine overdose. d. anxiety, irritability, and muscle tremors associated with caffeine overdose.

Answer: D Diff: 1 Page Ref: 268 31. Adenosine is a a. byproduct of cellular activity. b. retrograde neuromodulator. c. presynaptic antagonist. d. All of the above are correct Answer: D Diff: 2 Page Ref: 268–269 32. The ________ and ________ adenosine receptor subtypes are considered most important for understanding caffeine action. a. A1; A3 b. A1; A2A c. A1; A2B d. A2A; A3 Answer: B Diff: 2 Page Ref: 269 33. Caffeine’s effects on arousal and cognitive performance are mediated by a. increasing glutamate activity in the cortex by adenosine blockade. b. blocking GABAA receptors. c. increasing 5-HT activity in the raphe nucleus. d. modulating descending neurons from the pontine reticular formation.

Answer: B Diff: 2 Page Ref: 269–270 34. Tolerance to caffeine is believed to be mediated by ________ of ________ receptors. a. upregulation; GABAA b. downregulation; GABAA c. upregulation; adenosine d. downregulation; adenosine Answer: C Diff: 2 Page Ref: 270 35. Long-term use of caffeine is associated with a. caffeinism. b. an increased risk of cardiovascular disease. c. ischemia. d. dependence, but not addiction.

Answer: A Diff: 3 Page Ref: 2

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10.2 Discussion/Essay 1. Describe alcohol’s effects on the following neurotransmitters: GABA, glutamate, dopamine, and the opiates.

2. While alcohol effects on dopamine in the mesolimbic system are not completely described, review what we do know about how alcohol increases dopamine activity in this region.

3. Speculate on why such a small percentage of regular alcohol users actually become addicted to alcohol when compared to users of stimulants or opiates.

4. Describe nicotine’s mechanisms of action.

5. Discuss nicotine acetylcholine receptor upregulation and how this is believed to contribute to addiction.

6. Describe the role of adenosine in behavioral arousal.

7. Discuss caffeine effects on adenosine receptors and how this account for its stimulant action.

8. Why can we claim that although caffeine dependence can and does occur, caffeine addiction is not likely?

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