Dijk Derk-Jan, von Schantz Malcolm
Surrey Sleep Research Centre and Centre for Chronobiology, School of Biomedical and Molecular Sciences, University of Surrey, Guildford, United Kingdomd.
J Biol Rhythms. 2005 Aug;20(4):279-90. doi: 10.1177/0748730405278292.
Daily rhythms in sleep and waking performance are generated by the interplay of multiple external and internal oscillators. These include the light-dark and social cycles, a circadian hypothalamic oscillator oscillating virtually independently of behavior, and a homeostatic oscillator driven primarily by sleep-wake behavior. Both internal oscillators contribute to variation in many aspects of sleep and wakefulness (e.g., sleep timing and duration, REM sleep, non-REM sleep, REM density, sleep spindles, slow-wave sleep, electroencephalographic oscillations during wakefulness and sleep, and performance parameters, including attention and memory). The relative contribution of the oscillators varies greatly between these variables. Sleep and performance cannot be predicted by either oscillator independently but critically depend on their phase relationship and amplitude. The homeostatic oscillator feeds back onto the central pacemaker or its outputs. Thus, the amplitude of observed circadian variation in sleep and performance depends on how long we have been asleep or awake. During entrainment to external 24-h cycles, the opposing interplay between circadian and homeostatic changes in sleep propensity consolidates sleep and wakefulness. Some physiological correlates and mediators of both the circadian process (e.g., melatonin and hypocretin rhythms) and the homeostat (e.g., EEG, slow-wave activity, and adenosine release) have been established, offering targets for the development of countermeasures for circadian sleep and performance disorders. Interindividual differences in sleep timing, duration, and morning or evening preference are associated with changes of circadian or sleep homeostatic processes or both. Molecular genetic correlates, including polymorphisms in clock genes, of some of these interindividual differences are emerging.
睡眠和清醒表现的日常节律是由多个外部和内部振荡器的相互作用产生的。这些包括明暗周期和社会周期、一个几乎独立于行为振荡的昼夜节律下丘脑振荡器，以及一个主要由睡眠-清醒行为驱动的稳态振荡器。这两个内部振荡器都导致睡眠和清醒许多方面的变化（例如，睡眠时间和时长、快速眼动睡眠、非快速眼动睡眠、快速眼动密度、睡眠纺锤波、慢波睡眠、清醒和睡眠期间的脑电图振荡，以及包括注意力和记忆力在内的表现参数）。这些振荡器在这些变量之间的相对贡献差异很大。睡眠和表现不能由任何一个振荡器单独预测，而是严重依赖于它们的相位关系和振幅。稳态振荡器会反馈到中央起搏器或其输出上。因此，观察到的睡眠和表现的昼夜节律变化幅度取决于我们已经睡眠或清醒了多长时间。在与外部24小时周期同步的过程中，昼夜节律和睡眠倾向的稳态变化之间的相反相互作用巩固了睡眠和清醒。昼夜节律过程（例如，褪黑素和下丘脑分泌素节律）和稳态调节（例如，脑电图、慢波活动和腺苷释放）的一些生理相关因素和介质已经确定，为昼夜节律睡眠和表现障碍的对策开发提供了靶点。睡眠时间、时长以及早晨或晚上偏好的个体差异与昼夜节律或睡眠稳态过程或两者的变化有关。其中一些个体差异的分子遗传学相关因素，包括时钟基因多态性，正在显现出来。
