Corticotropin releasing hormone (CRH) is essential for stress adaptation by mediating hypothalamic-pituitary-adrenal (HPA) axis, behavioral and autonomic responses to stress. Activation of CRH neurons depends on neural afferents from the brain stem and limbic system, leading to sequential CRH release and synthesis. CRH transcription is required to restore mRNA and peptide levels, but termination of the response is essential to prevent pathology associated with chronic elevations of CRH and HPA axis activity. Inhibitory feedback mediated by glucocorticoids and intracellular production of the repressor, Inducible Cyclic AMP Early Repressor (ICER), limit the magnitude and duration of CRH neuronal activation. Induction of CRH transcription is mediated by the cyclic AMP/protein kinase A/cyclic AMP responsive element binding protein (CREB)-dependent pathways, and requires cyclic AMP-dependent nuclear translocation of the CREB co-activator, Transducer of Regulated CREB activity (TORC). This article reviews current knowledge on the mechanisms regulating CRH neuron activity.

中文翻译：

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CRH神经元的分子生理学

促肾上腺皮质激素释放激素 (CRH) 通过介导下丘脑-垂体-肾上腺 (HPA) 轴、对压力的行为和自主反应，对压力适应至关重要。CRH 神经元的激活依赖于来自脑干和边缘系统的神经传入，导致连续的 CRH 释放和合成。CRH 转录是恢复 mRNA 和肽水平所必需的，但终止反应对于预防与 CRH 和 HPA 轴活性慢性升高相关的病理学至关重要。由糖皮质激素介导的抑制性反馈和细胞内抑制因子、诱导型环 AMP 早期抑制因子 (ICER) 的产生限制了 CRH 神经元激活的幅度和持续时间。CRH 转录的诱导是由环 AMP/蛋白激酶 A/环 AMP 响应元件结合蛋白 (CREB) 依赖性途径介导的，并且需要 CREB ​​共激活剂、受调节的 CREB ​​活性转导器 (TORC) 的环 AMP 依赖性核易位）。本文回顾了目前关于调节 CRH 神经元活动的机制的知识。