Lesch K P, Laux G, Schulte H M, Pfüller H, Beckmann H
Department of Psychiatry, University of Würzburg, FRG.
Psychiatry Res. 1988 Apr;24(1):25-34. doi: 10.1016/0165-1781(88)90136-9.
To explore the integrity of the hypothalamic-pituitary-adrenal (HPA) system in major depressive disorder, 12 patients and normal controls matched for sex, age, and body weight received 100 micrograms synthetic human corticotropin-releasing hormone (hCRH) as an i.v. bolus dose. Compared to controls, depressed patients showed an elevation in baseline cortisol and a significant attenuation of net adrenocorticotropin (ACTH) responses, while cortisol secretion in response to hCRH was normal. These abnormalities in HPA axis function and apparent discordances in the interrelationships of ACTH and cortisol baseline and net stimulation responses between depressed patients and normal controls indicate, at least in part, a derangement of the glucocorticoid-dependent negative feedback circuitry and support the hypothesis that HPA hyperactivity in depression involves neurotransmitter-mediated hypothalamic hypersecretion of CRH.
为探究重度抑郁症患者下丘脑-垂体-肾上腺（HPA）系统的完整性，12名患者及在性别、年龄和体重方面与之匹配的正常对照者接受了100微克合成人促肾上腺皮质激素释放激素（hCRH）静脉推注剂量。与对照组相比，抑郁症患者的基线皮质醇升高，促肾上腺皮质激素（ACTH）净反应显著减弱，而对hCRH的皮质醇分泌正常。抑郁症患者与正常对照者之间HPA轴功能的这些异常以及ACTH和皮质醇基线及净刺激反应相互关系的明显不一致，至少部分表明糖皮质激素依赖性负反馈回路紊乱，并支持抑郁症中HPA功能亢进涉及神经递质介导的下丘脑CRH分泌过多这一假说。
