Effect of germ-free mice on monoamine neurotransmitter gene expression and anxiety-like behavior; further evidence of the gut-brain connection. Alexander Geiger
Studies have demonstrated gut microbiota are important for cognitive health, as revealed when gut microbiome balance is disrupted. Neurological, behavioral, and mental health issues can result. Questions arise as to what specific effects an abnormal microbiome have on the brain and, importantly, whether those effects can be reversed. The current study, represented by the visual abstract below, examined hippocampal monoamine neurotransmitter gene expression in mice with absent gut microbiota, and observed behavioral aspects, compared to mice with more normal gut microbiota (Pan et al. 2019). The researchers chose monoamine neurotransmitters as a promising biological indicator due to several previous studies linking this system to neuropsychiatric disorders. They compared Germ Free (GF) mice to Specific-Pathogen-Free (SPF) mice and found that 19 monoamine genes were expressed at different levels in GF mice. Additionally, GF mice portrayed much less anxiety than SPF mice, as measured using the open field test (OFT) and the novelty suppressed feeding test (NSF). The GF mice displayed higher locomotor activity and reduced latency for feeding compared to SPF mice. Finally, the researchers attempted to re-colonize gut microbiota in a set of GF mice (CGF) to reverse the effects of differential gene expression. However, CGF mice continued to show less anxiety compared with SPF mice, and only 50% of the monoamine neurotransmitter genes were successfully expressed to the same levels as SPF mice. Keywords: gut microbiota, gut-brain axis, monoamine neurotransmitters, GF/SPF mice, hippocampus
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