Decreasing a specific protein in the amygdala, an area of the brain involved in mood, creates antidepressant-like effects and reduces anxiety in mice. The findings, presented at a Monday, November 11Neuroscience 2013 press conference, the annual meeting of the Society for Neuroscience and the world’s largest source of emerging news about brain science and health, may help identify new molecular drug targets 30,000 scientists are attending this meeting. “Our data provide a new mechanism and location in the brain that can be used to study depression,” said lead author Yann Mineur, Ph.D., an Associate Research Scientist at Yale University School of Medicine. “These findings could lead to new tools to understand and diagnose depression, and might be the key to creating more effective antidepressants.” Previous studies show that drugs that block specific beta 2 nicotinic acetylcholine receptors (β2 nAChRs) can have antidepressant properties. To zero in on the role of this interaction, the researchers developed mice with localized reduction of β2 nAChRs expression and measured responses to social defeat stress tests. Dr. Mineur and his colleagues found that this change in the mouse amygdala appeared to protect against depression and anxiety in mice. The findings could guide researchers to a better understanding of the molecular mechanisms of depression and assist in the development of new drugs to treat mood disorders. When β2 nAChRs were knocked down in the hippocampus, there was no change in depression-like behavior or stress resilience in the social defeat test. These results suggest that decreasing nicotinic signaling through β2* nAChRs in the amygdala is antidepressant-like, likely due to the high level of tonic ACh input to this structure at baseline. The scientific presentation of Dr.
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