期刊
CELL METABOLISM
卷 25, 期 2, 页码 322-334出版社
CELL PRESS
DOI: 10.1016/j.cmet.2016.12.002
关键词
-
资金
- Funding Program for Next Generation World-Leading Researchers from the Japan Society for the Promotion of Science [LS070]
- MEXT of Japan [16H05128, 15H05932, 15K21744, 26118508, 26713009, 26290002, 15H01415, 26860159]
- U.S. NIH [R01NS40987, R01NS91066]
- Takeda Science Foundation
- Nakajima Foundation
- Uehara Memorial Foundation
- Brain Science Foundation
- Kowa Life Science Foundation
- Grants-in-Aid for Scientific Research [26118508, 26713009, 26290002, 16H05128, 15H01415, 26860159, 15K21744, 15H05932] Funding Source: KAKEN
Hypothalamic neuropeptide Y (NPY) elicits hunger responses to increase the chances of surviving starvation: an inhibition of metabolism and an increase in feeding. Here we elucidate a key central circuit mechanism through which hypothalamic NPY signals drive these hunger responses. GABAergic neurons in the intermediate and parvicellular reticular nuclei (IRt/PCRt) of the medulla oblongata, which are activated by NPY-triggered neural signaling from the hypothalamus, potentially through the nucleus tractus solitarius, mediate the NPY-induced inhibition of metabolic thermogenesis in brown adipose tissue (BAT) via their innervation of BAT sympathetic premotor neurons. Intriguingly, the GABAergic IRt/PCRt neurons innervating the BAT sympathetic premotor region also innervate the masticatory motor region, and stimulation of the IRt/PCRt elicits mastication and increases feeding as well as inhibits BAT thermogenesis. These results indicate that GABAergic IRt/PCRt neurons mediate hypothalamus-derived hunger signaling by coordinating both autonomic and feeding motor systems to reduce energy expenditure and to promote feeding.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据