Serotonin reciprocally regulates melanocortin neurons to modulate food intake
Serotonin reciprocally regulates melanocortin neurons to modulate food intake
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DOI：
10.1016/j.neuron.2006.06.004
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发表时间：
2006-07-20
期刊：
影响因子：
16.2
通讯作者：
Cowley, Michael A.
中科院分区：
文献类型：
--
作者：
Heisler, Lora K.;Jobst, Erin E.;Cowley, Michael A.
中枢多巴胺能系统调节食物摄入和体重的神经通路仍有待充分阐明。我们报告说，血清素，通过在aponin 1B受体（5-HT（1B）Rs）的行动，调节内源性释放的促效剂和拮抗剂的黑皮质素受体，这是一个核心组成部分的中央电路控制体重稳态。我们还表明，胡萝卜素诱导的食欲减退需要黑皮质素4，但不是黑皮质素3，受体的下游激活。这些结果确定了一个主要机制的能量平衡的β-肾上腺素能调节，并提供了一个例子，中枢来源的信号，β-肾上腺素能调节黑皮质素受体激动剂和拮抗剂以类似的方式外周肥胖信号。
The neural pathways through which central serotonergic systems regulate food intake and body weight remain to be fully elucidated. We report that serotonin, via action at serotonin1B receptors (5-HT(1B)Rs), modulates the endogenous release of both agonists and antagonists of the melanocortin receptors, which are a core component of the central circuitry controlling body weight homeostasis. We also show that serotonin-induced hypophagia requires downstream activation of melanocortin 4, but not melanocortin 3, receptors. These results identify a primary mechanism underlying the serotonergic regulation of energy balance and provide an example of a centrally derived signal that reciprocally regulates melanocortin receptor agonists and antagonists in a similar manner to peripheral adiposity signals.