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首页> 外文期刊>Pharmacology, Biochemistry and Behavior >Multiple feedback mechanisms activating corticotropin-releasing hormone system in the brain during stress.
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Multiple feedback mechanisms activating corticotropin-releasing hormone system in the brain during stress.

机译：在应激期间，多种反馈机制可激活大脑中促肾上腺皮质激素释放激素系统。

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Stress-associated disorders such as melancholic depression are characterized by persistent hypothalamic-pituitary-adrenocortical (HPA) axis activation and intensive anxiety. Corticotropin-releasing hormone (CRH) appears to play an essential role in pathophysiology of such disorders. In an attempt to elucidate possible mechanisms underlying persistent activation of CRH in the central nervous system (CNS), we examined responses of hypothalamic and extrahypothalamic CRH systems to the stressors (immobilization stress or psychological stress) and interactions between these CRH systems and glucocorticoids in rats. We propose multiple feedback loops activating central CRH system: (1) attenuation of glucocorticoid-induced negative feedback on the activity of the hypothalamic and brainstem nuclei during chronic stress, (2) autoregulation of CRH biosynthesis in the hypothalamic paraventricular nucleus (PVN) through up-regulation of Type-1 CRH receptor (CRHR-1), and (3) glucocorticoid-mediated positive effects on the amygdaloid CRH system. Stress initially activates the hypothalamic CRH system, resulting in the hypersecretion of glucocorticoids from the adrenal gland. In addition, the psychological component of the stressor stimulates the amygdaloid CRH system. In the chronic phase of stress, down-regulation of GR in the PVN and other brain structures such as the locus coeruleus (LC) fails to restrain hyperfunction of the HPA axis, and persistent activation of the HPA axis further up-regulates the amygdaloid CRH system. Thus, the hypothalamic and the amygdaloid CRH systems cooperatively constitute stress-responsive, anxiety-producing neurocircuitry during chronic stress, which is responsible for the clinical manifestations of stress-associated disorders. Effects of tricyclic antidepressants (TCAs), which appear to mitigate the above mentioned multiple feedback loop forming the vicious circle to activate central CRH systems, will also be discussed.
机译：与压力相关的疾病（例如忧郁症抑郁症）的特征在于持续的下丘脑-垂体-肾上腺皮质激素（HPA）轴激活和强烈焦虑。促肾上腺皮质激素释放激素（CRH）似乎在此类疾病的病理生理中起着至关重要的作用。为了阐明潜在的中枢神经系统（CNS）中CRH持续激活的可能机制，我们研究了下丘脑和下丘脑CRH系统对应激源的反应（固定应激或心理应激）以及这些CRH系统与大鼠糖皮质激素之间的相互作用。我们提出了多个激活中央CRH系统的反馈回路：（1）在慢性应激期间，糖皮质激素诱导的对下丘脑和脑干核活动的负反馈的减弱;（2）下丘脑室旁核（PVN）中CRH生物合成的自动调节-1型CRH受体（CRHR-1）的调节，以及（3）糖皮质激素介导的对杏仁状CRH系统的积极作用。压力最初会激活下丘脑CRH系统，导致肾上腺分泌糖皮质激素过多。此外，应激源的心理成分会刺激杏仁状CRH系统。在慢性应激阶段，PVN和其他大脑结构（例如蓝斑轨迹（LC））中GR的下调无法抑制HPA轴的功能亢进，而HPA轴的持续激活进一步上调了杏仁状CRH系统。因此，下丘脑和杏仁状CRH系统在慢性应激期间共同构成应激反应，产生焦虑的神经回路，这是应激相关疾病的临床表现的原因。也将讨论三环类抗抑郁药（TCA）的作用，该作用似乎减轻了上述形成恶性循环的多重反馈回路，从而激活了中央CRH系统。

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