Stenberg D
Institute of Biomedicine/Physiology, University of Helsinki, Helsinki, Finland.
Cell Mol Life Sci. 2007 May;64(10):1187-204. doi: 10.1007/s00018-007-6530-3.
Sleep is regulated by homeostatic and circadian factors, and the regulation of sleep of mammals shares many molecular properties with the rest state of submammalian species. Several brain structures take part in waking: the basal forebrain, posterior and lateral hypothalamus, and nuclei in the tegmentum and pons. Active sleep mechanisms are located to the preoptic/anterior hypothalamic area. In addition to acetylcholine and monoamines, glutamate and hypocretin/orexin are important waking factors. Gamma-aminobutyric acid and several peptide factors, including cytokines, growth hormone-releasing hormone and prolactin, are related to sleep promotion. Adenosine is an important homeostatic sleep factor acting in basal forebrain and preoptic areas through A1 and A2A receptors. Prolonged waking activates inducible nitric oxide synthase in the basal forebrain, which through energy depletion causes adenosine release and recovery sleep. Numerous genes have been found differentially displayed in waking compared with sleep, and they relate to neural transmission, synaptic plasticity, energy metabolism and stress protection. The genetic background of a few sleep disorders has been solved.
睡眠受稳态和昼夜节律因素调节，哺乳动物的睡眠调节与亚哺乳动物物种的静息状态具有许多分子特性。几个脑结构参与觉醒过程：基底前脑、下丘脑后部和外侧以及被盖和脑桥中的核团。主动睡眠机制位于视前区/下丘脑前部区域。除乙酰胆碱和单胺外，谷氨酸和下丘脑分泌素/食欲素是重要的觉醒因子。γ-氨基丁酸和几种肽类因子，包括细胞因子、生长激素释放激素和催乳素，与促进睡眠有关。腺苷是一种重要的稳态睡眠因子，通过A1和A2A受体作用于基底前脑和视前区。长时间觉醒会激活基底前脑中的诱导型一氧化氮合酶，其通过能量消耗导致腺苷释放并引发恢复性睡眠。与睡眠相比，已发现许多基因在觉醒状态下有差异表达，它们与神经传递、突触可塑性、能量代谢和应激保护有关。一些睡眠障碍的遗传背景已被破解。
