期刊
JOURNAL OF NEUROSCIENCE
卷 31, 期 17, 页码 6449-6456出版社
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.6144-10.2011
关键词
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资金
- UNCF/Merck
- National Institute of Mental Health (NIMH) [P50MH060451]
- National Institute on Drug Abuse
- Blue Gator Foundation
- McKnight Foundation
- National Alliance for Research on Schizophrenia and Depression
- National Institutes of Health [P50MH060451]
- Safra Foundation
- Meyerhoff Scholarship Program
Alterations in anxiety-related processing are observed across many neuropsychiatric disorders, including bipolar disorder. Though polymorphisms in a number of circadian genes confer risk for this disorder, little is known about how changes in circadian gene function disrupt brain circuits critical for anxiety-related processing. Here we characterize neurophysiological activity simultaneously across five limbic brain areas (nucleus accumbens, amygdala, prelimbic cortex, ventral hippocampus, and ventral tegmental area) as wild-type (WT) mice and mice with a mutation in the circadian gene, CLOCK (Clock-Delta 19 mice) perform an elevated zero maze task. In WT mice, basal limbic gamma oscillatory synchrony observed before task performance predicted future anxiety-related behaviors. Additionally, dynamic changes in limbic gamma oscillatory synchrony were observed based on the position of WT mice in the zero maze. Clock-Delta 19 mice, which displayed an increased propensity to enter the open section of the elevated maze, showed profound deficits in these anxiety-related circuit processes. Thus, our findings link the anxiety-related behavioral deficits observed in Clock-Delta 19 mice with dysfunctional gamma oscillatory tuning across limbic circuits and suggest that alterations in limbic oscillatory circuit function induced by circadian gene polymorphisms may contribute to the behavioral manifestations seen in bipolar mania.
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