Holsboer F, von Bardeleben U, Buller R, Heuser I, Steiger A
Psychiatrische Universitätsklinik, Universität Mainz, Germany.
Horm Metab Res Suppl. 1987;16:80-8.
Alterations in baseline and challenged pituitary-adrenocortical function constitute the most extensively studied abnormalities in affective disorders. The recent availability of corticotropin-releasing hormone (CRH) for clinical studies opened the possibility to further investigate pathophysiology underlying aberrant ACTH and cortisol secretion. When injected to depressives CRH induces a blunted ACTH but normal cortisol release. Similar response patterns were observed among patients with panic disorder and alcoholism. In these diseases, enhanced baseline pituitary adrenocortical activity appears to be driven by a CNS disturbance resulting in overactive CRH secreting neurons. In addition to these endocrine findings we observed among normal controls suppressed nocturnal slow-wave sleep and growth hormone surges during infusions of CRH. Our clinical investigations with CRH support that this neuropeptide is involved in mediation of several neuroendocrine and behavioral changes frequently observed in depressive syndromes.
基线和激发状态下垂体 - 肾上腺皮质功能的改变是情感障碍中研究最为广泛的异常情况。促肾上腺皮质激素释放激素（CRH）近期可用于临床研究，这为进一步探究促肾上腺皮质激素（ACTH）和皮质醇分泌异常背后的病理生理学机制提供了可能。给抑郁症患者注射CRH时，会诱导出ACTH反应迟钝但皮质醇释放正常的情况。在恐慌症和酒精中毒患者中也观察到了类似的反应模式。在这些疾病中，增强的基线垂体肾上腺皮质活动似乎是由中枢神经系统紊乱驱动的，导致CRH分泌神经元过度活跃。除了这些内分泌学发现外，我们在正常对照中观察到，在输注CRH期间夜间慢波睡眠受到抑制，生长激素激增。我们对CRH的临床研究支持这种神经肽参与介导了抑郁综合征中常见的几种神经内分泌和行为变化。
