AMP-Activated Kinase Links Serotonergic Signaling to Glutamate Release for Regulation of Feeding Behavior in C. elegans

被引：61

作者：

Cunningham, Katherine A. ^{[1
,2
,3
]}

Hua, Zhaolin ^{[1
,4
]}

Srinivasan, Supriya ^{[5
,6
]}

Liu, Jason ^{[1
,2
,3
]}

Lee, Brian H. ^{[1
,2
,3
]}

Edwards, Robert H. ^{[1
,4
]}

Ashrafi, Kaveh ^{[1
,2
,3
]}

机构：

[1] Univ Calif San Francisco, Dept Physiol, San Francisco, CA 94158 USA

[2] Univ Calif San Francisco, Cardiovasc Res Inst, San Francisco, CA 94158 USA

[3] Univ Calif San Francisco, Ctr Diabet, San Francisco, CA 94158 USA

[4] Univ Calif San Francisco, Dept Neurol, San Francisco, CA 94158 USA

[5] Scripps Res Inst, Dept Physiol Chem, La Jolla, CA 92037 USA

[6] Scripps Res Inst, Dorris Neurosci Ctr, La Jolla, CA 92037 USA

来源：

CELL METABOLISM | 2012年 / 16卷 / 01期

基金：

美国国家卫生研究院;

关键词：

NEMATODE CAENORHABDITIS-ELEGANS; SYNAPTIC-TRANSMISSION; ENERGY-BALANCE; PATHWAY; CIRCUIT; EXPRESSION; RECEPTOR; HYPOTHALAMUS; STARVATION; PROTEINS;

D O I：

10.1016/j.cmet.2012.05.014

中图分类号：

Q2 [细胞生物学];

学科分类号：

071013 [干细胞生物学];

摘要：

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.

引用

页码：113 / 121

页数：9

共 42 条

[1]

The Caenorhabditis elegans ems class homeobox gene ceh-2 is required for M3 pharynx motoneuron function [J].