Parabrachial CGRP Neurons Control Meal Termination.
Parabrachial CGRP Neurons Control Meal Termination.
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DOI：
10.1016/j.cmet.2016.04.006
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发表时间：
2016-05-10
期刊：
影响因子：
29
通讯作者：
Palmiter RD
中科院分区：
文献类型：
--
作者：
Campos CA;Bowen AJ;Schwartz MW;Palmiter RD
臂旁外侧核是导致厌食的内脏信号的管道。我们之前发现了位于外侧臂旁核（PBel）的神经元子集，这些神经元表达降钙素基因相关肽（CGRP）并在被疾病模拟物激活时抑制进食。我们在这里报告，在其他方面正常的小鼠中，CGRP 神经元的功能性失活显着增加了进餐量，进餐频率以补偿方式减少，并使小鼠对进餐相关的饱腹感肽的厌食作用不敏感。此外，CGRP 神经元直接受促食欲下丘脑 AgRP 神经元的支配，光刺激提供 PBel 的 AgRP 纤维可通过抑制 CGRP 神经元延迟饱足感，从而导致 AgRP 驱动的食欲亢进。通过确定 CGRP 神经元在控制进餐终止中的作用以及作为 AgRP 神经元引发的进食的下游介质，这些发现确定了饥饿和饱腹感回路相互作用以控制进食行为的节点。
The lateral parabrachial nucleus is a conduit for visceral signals that cause anorexia. We previously identified a subset of neurons located in the external lateral parabrachial nucleus (PBel) that express calcitonin gene-related peptide (CGRP) and inhibit feeding when activated by illness mimetics. We report here that in otherwise normal mice, functional inactivation of CGRP neurons markedly increases meal size, with meal frequency being reduced in a compensatory manner, and renders mice insensitive to the anorexic effects of meal-related satiety peptides. Furthermore, CGRP neurons are directly innervated by orexigenic hypothalamic AgRP neurons, and photostimulation of AgRP fibers supplying the PBel delays satiation by inhibiting CGRP neurons, thereby contributing to AgRP-driven hyperphagia. By establishing a role for CGRP neurons in the control of meal termination and as a downstream mediator of feeding elicited by AgRP neurons, these findings identify a node in which hunger and satiety circuits interact to control feeding behavior.