Sleep. A physiologic role for IL-1 beta and TNF-alpha.

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 or TNF-alpha induces increased non-rapid eye movement (NREMS). Inhibition TNF reduces spontaneous sleep. There is a diurnal rhythm mRNA brain with highest levels occurring during peak periods. Mice lacking either the 55-kD receptor type I less than do strain controls. part larger biochemical cascade regulation; other somnogenic substances this include growth hormone-releasing hormone nitric oxide. Several additional inhibitory feedback mechanisms, some which inhibit TNF. A major challenge to research define how where these molecular steps produce