کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2792981 | 1155102 | 2012 | 9 صفحه PDF | دانلود رایگان |

SummarySerotonergic 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 SIM1, 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.
Graphical AbstractFigure optionsDownload high-quality image (126 K)Download as PowerPoint slideHighlights
► C. elegans counterparts of obesity genes mediate serotonergic feeding behavior
► Serotonin signaling causes inhibition of AMP-activated kinase
► Inhibition of AMP-activated kinase promotes glutamatergic release
Journal: - Volume 16, Issue 1, 3 July 2012, Pages 113–121