The versatility of the vagus

The versatility of the vagus
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DOI:
10.1016/j.physbeh.2009.01.009
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发表时间:
2009-07-14
影响因子:
2.9
通讯作者:
Dockray, Graham J.
Dockray, Graham J.
中科院分区:
医学3区
文献类型:
--
作者:
Dockray, Graham J.

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肠道是控制食物摄入的外周信号网络的几个器官之一。迷走神经的传入神经元为肠道信号提供了一条重要的通路,肠道信号通过触发从脑干到下丘脑的上行通路而起作用。最近的工作表明,存在的机制,在迷走神经传入神经元的水平,以调节胃肠道饱足信号的影响。因此,众所周知的饱腹感激素胆囊收缩素(CCK)不仅刺激这些神经元的放电,而且控制它们对已知影响食物摄入的G蛋白偶联受体和肽神经递质的表达。当血浆CCK浓度低时,例如在禁食时,大麻素(CB)-1和黑色素浓集激素(MCH)-1受体的迷走传入神经元的表达增加。通过进食释放CCK导致两种受体表达的快速下调和Y2受体表达的增加。在禁食时,这些神经元中刺激食欲的神经肽递质MCH的表达也增加,饱腹肽可卡因和安非他明调节转录物(CART p)的表达降低;内源性CCK降低MCH表达并刺激CART表达。胃促食欲激素ghrelin至少部分地通过将磷酸化CREB排除在细胞核之外来阻断CCK的这些作用。这些数据表明,CCK作为一个看门人,以确定其他神经内分泌信号的能力,通过迷走神经传入神经元影响食物摄入。(C)2009 Elsevier Inc. All rights reserved.
The gut is one of several organs contributing to the peripheral signalling network that controls food intake. Afferent neurons of the vagus nerve provide an important pathway for gut signals that act by triggering ascending pathways from the brain stem to hypothalamus. Recent work indicates the existence of mechanisms operating at the level of vagal afferent neurons to modulate the effect of gastrointestinal satiety signals. Thus, the well known satiety hormone cholecystokinin (CCK) not only stimulates the discharge of these neurons but also controls their expression of both G-protein coupled receptors and peptide neurotransmitters known to influence food intake. When plasma CCK concentrations are low e.g. in fasting, the expression by vagal afferent neurons of cannabinoid (CB)-1 and melanin concentrating hormone (MCH)-1 receptors is increased. Release of CCK by feeding leads to a rapid down-regulation of expression of both receptors and to increased expression of Y2 receptors. In fasting, there is also increased expression in these neurons of the appetite-stimulating neuropeptide transmitter MCH, and depressed expression of the satiety-peptide cocaine and amphetamine regulated transcript (CARTp); endogenous CCK decreases MCH expression and stimulates CART expression. The gastric orexigenic hormone ghrelin blocks these actions of CCK at least in part by excluding phosphoCREB from the nucleus. The data suggest that CCK acts as a gatekeeper to determine the capacity of other neuroendocrine signals to act via vagal afferent neurons to influence food intake. (C) 2009 Elsevier Inc. All rights reserved.