Beuckmann Carsten T, Yanagisawa Masashi
Howard Hughes Medical Institute and Department of Molecular Genetics, University of Texas, Southwestern Medical Center, 5323 Harry Hines Blvd., Dallas, TX 75390-9050, USA.
J Mol Med (Berl). 2002 Jun;80(6):329-42. doi: 10.1007/s00109-002-0322-x. Epub 2002 Apr 5.
The neuropeptides orexin A and orexin B (also called hypocretin 1 and 2) were recently discovered by a "reverse pharmacology" approach as ligands for two previously orphan G protein coupled receptors: orexin receptors 1 and 2. Neurons producing orexins are located exclusively in the lateral hypothalamic area but project broadly to various parts of the brain, and they have been implicated in the control of energy homeostasis and arousal maintenance. The orexin receptors are also broadly expressed in the central nervous system. Murine and canine models suggest that defective signaling in the orexin system is responsible for the sleep/wake disorder narcolepsy. Although narcoleptic patients rarely have genetic defects in the orexin system, they lack these neuropeptides in the brain and cerebrospinal fluid, indicating that human narcolepsy is an orexin deficiency syndrome in the majority of cases. A connection between sleep/wake regulation and energy homeostasis is hypothesized with orexin neuropeptides as a molecular link.
神经肽食欲素A和食欲素B(也称为下丘脑泌素1和2)最近通过“反向药理学”方法被发现,它们是两种先前未明确配体的G蛋白偶联受体——食欲素受体1和2的配体。产生食欲素的神经元仅位于下丘脑外侧区,但广泛投射到大脑的各个部位,它们与能量稳态的控制和觉醒维持有关。食欲素受体在中枢神经系统中也广泛表达。小鼠和犬类模型表明,食欲素系统中的信号缺陷是导致睡眠/觉醒障碍发作性睡病的原因。尽管发作性睡病患者在食欲素系统中很少有基因缺陷,但他们的大脑和脑脊液中缺乏这些神经肽,这表明在大多数情况下,人类发作性睡病是一种食欲素缺乏综合征。人们推测睡眠/觉醒调节与能量稳态之间存在联系,食欲素神经肽是其中的分子纽带。