Corticotropin-releasing hormone inhibits melatonin secretion in healthy volunteers - A potential link to low-melatonin syndrome in depression?
Corticotropin-releasing hormone inhibits melatonin secretion in healthy volunteers - A potential link to low-melatonin syndrome in depression?
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DOI：
10.1159/000127186
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发表时间：
1997-04-01
影响因子：
4.1
通讯作者：
Wiedemann, K
中科院分区：
文献类型：
--
作者：
Kellner, M;Yassouridis, A;Wiedemann, K
下丘脑-垂体-肾上腺皮质（HPA）系统和褪黑激素分泌之间的相互作用已被证明，但只有褪黑激素对HPA系统的活性的影响已被研究man. Alterations褪黑激素分泌的改变被描述为低褪黑激素综合征已被证明在患有抑郁症发作的患者，和褪黑激素分泌的抑制因子已被假定。我们研究了促肾上腺皮质激素释放激素（CRH）是否也能抑制健康志愿者的褪黑激素分泌，CRH被认为与抑郁症患者的HPA异常有关。在双盲研究设计中，10名健康男性志愿者从08.00至18.00小时每小时接受随机静脉注射，其中含有10 μ g人CRH、1 μ g促肾上腺皮质激素（ACTH）或安慰剂以模拟脉动激素分泌。记录治疗过程中血浆褪黑素和皮质醇的反应及治疗后夜间睡眠脑电图。CRH的管理减少褪黑激素分泌显着低于安慰剂和ACTH管理后获得的值。与安慰剂和CRH相比，ACTH显著增强皮质醇分泌。脑电图睡眠参数显示无治疗效应。我们的研究结果表明，CRH对正常人松果体褪黑素的分泌有抑制作用，但不支持通过释放皮质醇的机制。排除了夜间睡眠结构变化引起的继发性激素效应。进一步研究CRH对褪黑激素分泌的作用以及HPA系统和松果体之间的相互反馈可能会扩展我们对神经内分泌改变介导的适应性应激反应和最终参与抑郁症发病机制的认识。
Interactions between the hypothalamic-pituitary-adrenocortical (HPA) system and melatonin secretion have been demonstrated, but only the effects of melatonin on the activity of the HPA system have been studied in man. Alterations of melatonin secretion described as low-melatonin syndrome have been demonstrated in patients suffering from a major depressive episode, and an inhibitory factor on melatonin secretion has been postulated. We investigated whether corticotropin-releasing hormone (CRH), which is thought to be involved in HPA abnormalities in depressed patients, can also suppress melatonin secretion in healthy volunteers. Ten healthy male human volunteers in a double-blind study design received randomized hourly intravenous injections from 08.00 to 18.00 h that contained 10 mu g human CRH, 1 mu g adrenocorticotropic hormone (ACTH), or placebo to simulate pulsatile hormone secretion. Plasma melatonin and cortisol responses during the treatment and nocturnal sleep electroencephalograms after the treatment were recorded. Administration of CRH reduced melatonin secretion significantly below values obtained after administration of placebo and ACTH. Cortisol secretion was significantly enhanced by ACTH in comparison to both placebo and CRH. Electroencephalographic sleep parameters revealed no treatment effects. Our findings suggest that CRH has an inhibitory effect on the pineal secretion of melatonin in normal man. A mechanism via a release of cortisol was not supported by our results. Secondary hormonal effects from changes in nocturnal sleep architecture were excluded. Further investigation of the action of CRH on melatonin secretion as well as the mutual feedback between the HPA system and the pineal gland may extend our knowledge of neuroendocrine alterations mediating the adaptive response to stress and the eventual involvement in the pathogenesis of depression.