Sleep - A physiologic role for IL-1β and TNF-αa

James M. Krueger, Jidong Fang, Ping Taishi, Zutang Chen, Tetsuya Kushikata, Janos Gardi

Research output: Contribution to journalArticle

146 Scopus citations

Abstract

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 languageEnglish (US)
Pages (from-to)148-159
Number of pages12
JournalAnnals of the New York Academy of Sciences
Volume856
DOIs
StatePublished - Jan 1 1998

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)
  • Biochemistry, Genetics and Molecular Biology(all)
  • History and Philosophy of Science

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