Krueger James M, Fang Jidong, Taishi Ping, Chen Zutang, Kushikata Tetsuya, Gardi Janos
Department of Veterinary and Comparative Anatomy, Pharmacology and Physiology, Washington State University, Pullman, Washington 99164-6520, USA.
Ann N Y Acad Sci. 1998 Sep 29;856:148-159. doi: 10.1111/j.1749-6632.1998.tb08323.x.
Interleukin-1 beta (IL-1 beta) and tumor necrosis factor-alpha (TNF-alpha) are involved in physiologic sleep regulation. Administration of exogenous IL-1 beta or TNF-alpha induces increased non-rapid eye movement sleep (NREMS). Inhibition of IL-1 or TNF reduces spontaneous sleep. There is a diurnal rhythm of TNF-alpha mRNA and IL-1 beta mRNA in brain with highest levels occurring during peak sleep periods. Mice lacking either the TNF 55-kD receptor or the IL-1 type I receptor sleep less than do strain controls. IL-1 beta and TNF-alpha are part of a larger biochemical cascade involved in sleep regulation; other somnogenic substances in this cascade include growth hormone-releasing hormone and nitric oxide. Several additional substances are involved in inhibitory feedback mechanisms, some of which inhibit IL-1 and TNF. A major challenge to sleep research is to define how and where these molecular steps produce sleep.
白细胞介素-1β（IL-1β）和肿瘤坏死因子-α（TNF-α）参与生理性睡眠调节。给予外源性IL-1β或TNF-α会导致非快速眼动睡眠（NREMS）增加。抑制IL-1或TNF会减少自发睡眠。大脑中TNF-α mRNA和IL-1β mRNA存在昼夜节律，在睡眠高峰期水平最高。缺乏TNF 55-kD受体或IL-1 I型受体的小鼠比品系对照睡眠少。IL-1β和TNF-α是参与睡眠调节的更大生化级联反应的一部分；该级联反应中的其他促眠物质包括生长激素释放激素和一氧化氮。还有几种其他物质参与抑制性反馈机制，其中一些抑制IL-1和TNF。睡眠研究的一个主要挑战是确定这些分子步骤如何以及在何处产生睡眠。
