Journal
CELL METABOLISM
Volume 16, Issue 1, Pages 113-121Publisher
CELL PRESS
DOI: 10.1016/j.cmet.2012.05.014
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Funding
- National Institutes of Health (NIH) [HL007731]
- Burroughs Wellcome Fund
- National Institute of Mental Health [MH50712]
- National Institute on Drug Abuse [DA10154]
- NIH National Center for Research Resources (NCRR)
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Serotonergic regulation of feeding behavior has been studied intensively, both for an understanding of the basic neurocircuitry of energy balance in various organisms and as a therapeutic target for human obesity. However, its underlying molecular mechanisms remain poorly understood. Here, we show that neural serotonin signaling in C. elegans modulates feeding behavior through inhibition of AMP-activated kinase (AMPK) in interneurons expressing the C. elegans counterpart of human S1M1, a transcription factor associated with obesity. In turn, glutamatergic signaling links these interneurons to pharyngeal neurons implicated in feeding behavior. We show that AMPK-mediated regulation of glutamatergic release is conserved in rat hippocampal neurons. These findings reveal cellular and molecular mediators of serotonergic signaling.
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