A spoonful of sugar: feedback signals of energy stores and corticosterone regulate responses to chronic stress
A spoonful of sugar: feedback signals of energy stores and corticosterone regulate responses to chronic stress
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DOI：
10.1016/s0031-9384(03)00100-8
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发表时间：
2003-06-01
影响因子：
2.9
通讯作者：
Bhatnagar, S
中科院分区：
文献类型：
--
作者：
Dallman, MF;Akana, SF;Bhatnagar, S
为了开始了解慢性压力对食物摄入和能量储存的影响，必须首先了解下丘脑-垂体-肾上腺（HPA）轴和糖皮质激素（GC）活动增加对身体和大脑的影响。我们提出了两个主要的系统，都是GC敏感：代谢反馈，抑制和直接中央GC驱动。在基础条件下，代谢反馈信号到大脑是占主导地位的，虽然GC注入侧脑室阻断代谢反馈的影响。慢性应激激活GC分泌和脑核GC受体占用，显着改变这两个主要的皮质类固醇激活系统之间的正常关系。这些信号的相对强度的应激源诱导的开关决定了随后的压力反应（行为，神经内分泌和自主神经流出）的大脑调节。GC的代谢反馈效应通过肾上腺切除大鼠的自愿蔗糖摄入来模拟，并且实验表明代谢反馈也抑制应激诱导的对脑的直接GC驱动。我们推测，外周和中央GC敏感的信号系统之间的相互作用可能是通过内源性阿片类药物的输入对促肾上腺皮质激素释放因子（CRF）神经元的抑制作用耦合。(C)2003年爱思唯尔科学公司All rights reserved.
To begin to understand the effects of chronic stress on food intake and energy stores, the effects of increased activity in the hypothalamo-pituitary-adrenal (HPA) axis and glucocorticoids (GCs) on the body and brain must first be understood. We propose two major systems that are both GC sensitive: a metabolic feedback that is inhibitory and a direct central GC drive. Under basal conditions, the metabolic feedback signal to brain is dominant, although infusion of GC into a lateral brain ventricle blocks the effects of the metabolic feedback. Chronic stress activates GC secretion and brain nuclear GC receptor occupancy, markedly changing the normal relationships between these two major corticosteroid-activated systems. The stressor-induced switch in the relative strengths of these signals determines subsequent brain regulation of stress responses (behavioral, neuroendocrine and autonomic outflows). The metabolic feedback effects of GCs are mimicked by voluntary sucrose ingestion in adrenalectomized rats, and experiments suggest that the metabolic feedback also inhibits the stressor-induced direct GC drive on brain. We speculate that the interaction between peripheral and central GC-sensitive signaling systems may be coupled through the inhibitory actions of endogenous opiatergic inputs on corticotropin-releasing factor (CRF) neurons. (C) 2003 Elsevier Science Inc. All rights reserved.