Sleep -: A physiologic role for IL-1β and TNF-α

被引：153

作者：

Krueger, JM ^{[1
]}

Fang, JD ^{[1
]}

Ping, TS ^{[1
]}

Chen, ZT ^{[1
]}

Kushikata, T ^{[1
]}

Gardi, J ^{[1
]}

机构：

[1] Washington State Univ, Coll Vet Med, Dept Vet & Comparat Anat Pharmacol & Physiol, Pullman, WA 99164 USA

来源：

MOLECULAR MECHANISMS OF FEVER | 1998年 / 856卷

关键词：

D O I：

10.1111/j.1749-6632.1998.tb08323.x

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

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.

引用

页码：148 / 159

页数：12

共 75 条

[61] An interleukin-1 receptor fragment inhibits spontaneous sleep and muramyl dipeptide-induced sleep in rabbits [J].