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急性给予皮质醇可提高人类的睡眠强度。

Acute cortisol administration promotes sleep intensity in man.

作者信息

Friess Elisabeth, Tagaya Hirokuni, Grethe Claus, Trachsel Lorenz, Holsboer Florian

机构信息

Max Planck Institute of Psychiatry, Munich, Germany.

出版信息

Neuropsychopharmacology. 2004 Mar;29(3):598-604. doi: 10.1038/sj.npp.1300362.

Abstract

The neuronal mechanisms of sleep generation, in particular synchronization of brain activity in the process of non-rapid-eye movement (non-REM) sleep, has been elucidated in the past decade. A previous study of our group showed that acute administration of cortisol is known to increase slow-wave sleep and suppress rapid-eye movement (REM) sleep in man. To further elucidate the non-REM sleep-promoting effects of cortisol with respect to the synchronization of cortical activity, it is important to establish a sleep-state-specific quantitative EEG analysis. We therefore investigated the effects of repetitive injections of hydrocortisone on spectral composition of sleep EEG in 10 healthy male young volunteers. In addition, we performed high-frequency blood samplings to assess the relation between changes in the sleep EEG and sleep-associated secretion of growth hormone (GH). Cortisol administration resulted in a significant increase in highly synchronized EEG activity including delta and theta frequencies, according to a higher amount of slow-wave sleep. This effect predominated in the first few hours of night sleep. REM sleep was decreased, which appeared to be secondary to the lengthened first sleep cycle. The cortisol-induced stimulation of GH release did not occur in correspondence with the increased slow-wave activity. In view of the sleep impairing properties of corticotropin-releasing hormone (CRH) and the sleep-promoting function of GH-releasing hormone, it appears likely that a negative feedback inhibition of endogenous CRH was the key mechanism mediating the observed results. The cortisol-induced effects on sleep intensity and sleep-associated GH secretion appeared to be driven by different mechanisms.

摘要

在过去十年中,睡眠产生的神经元机制,尤其是非快速眼动(non-REM)睡眠过程中大脑活动的同步化机制已得到阐明。我们团队之前的一项研究表明,已知急性给予皮质醇会增加人类的慢波睡眠并抑制快速眼动(REM)睡眠。为了进一步阐明皮质醇在促进非快速眼动睡眠方面对皮质活动同步化的影响,建立一种针对睡眠状态的定量脑电图分析方法很重要。因此,我们研究了对10名健康男性青年志愿者重复注射氢化可的松对睡眠脑电图频谱组成的影响。此外,我们进行了高频血液采样,以评估睡眠脑电图变化与睡眠相关生长激素(GH)分泌之间的关系。根据慢波睡眠量的增加,给予皮质醇导致包括δ和θ频率在内的高度同步化脑电图活动显著增加。这种效应在夜间睡眠的最初几个小时最为明显。快速眼动睡眠减少,这似乎是由于第一个睡眠周期延长所致。皮质醇诱导的生长激素释放刺激与慢波活动增加并不对应。鉴于促肾上腺皮质激素释放激素(CRH)的睡眠损害特性以及生长激素释放激素的促睡眠功能,内源性CRH的负反馈抑制似乎是介导观察结果的关键机制。皮质醇对睡眠强度和睡眠相关生长激素分泌的影响似乎由不同机制驱动。

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