Mieda Michihiro
Department of Molecular Neuroscience and Integrative Physiology, Graduate School of Medical Sciences, Kanazawa University, 13-1 Takara-Machi, Kanazawa, Ishikawa 920-8640, Japan.
Neurosci Res. 2017 May;118:56-65. doi: 10.1016/j.neures.2017.03.015. Epub 2017 May 16.
Orexin A and orexin B are hypothalamic neuropeptides initially identified as endogenous ligands for two orphan G-protein coupled receptors (GPCRs). A deficiency of orexin signaling results in the sleep disorder narcolepsy-cataplexy in humans, dogs, and rodents, a sleep disorder characterized by excessive daytime sleepiness and cataplexy. Multiple approaches, including molecular genetic, electrophysiological, pharmacological, and neuroanatomical studies have suggested that orexins play critical roles in the maintenance of wakefulness by regulating the function of monoaminergic and cholinergic neurons that are implicated in the regulation of wakefulness. Here, I review recent advances in the understanding of how orexins regulate sleep/wakefulness and prevent narcolepsy.
食欲素A和食欲素B是下丘脑神经肽，最初被鉴定为两种孤儿G蛋白偶联受体（GPCR）的内源性配体。食欲素信号传导的缺陷会导致人类、狗和啮齿动物出现发作性睡病-猝倒这一睡眠障碍，其特征为白天过度嗜睡和猝倒。包括分子遗传学、电生理学、药理学和神经解剖学研究在内的多种方法表明，食欲素通过调节与觉醒调节有关的单胺能和胆碱能神经元的功能，在维持觉醒中发挥关键作用。在此，我综述了在理解食欲素如何调节睡眠/觉醒以及预防发作性睡病方面的最新进展。
