Interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) are involved in physiologic sleep regulation. Administration of exogenous IL-1β or TNF-α induces increased non-rapid eye movement sleep (NREMS). Inhibition of IL-1 or TNF reduces spontaneous sleep. There is a diurnal rhythm of TNF-α mRNA and IL-1β 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-1β and TNF-α 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.
|Original language||English (US)|
|Number of pages||12|
|Journal||Annals of the New York Academy of Sciences|
|State||Published - Jan 1 1998|
All Science Journal Classification (ASJC) codes
- Biochemistry, Genetics and Molecular Biology(all)
- History and Philosophy of Science