Journal
AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY
Volume 285, Issue 1, Pages R99-R109Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpregu.00609.2002
Keywords
electroencephalogram; cytokine; slow-wave activity
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Funding
- NINDS NIH HHS [NS-31453] Funding Source: Medline
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Sleep is regulated in part by the brain cytokine network, including tumor necrosis factor-alpha (TNF-alpha). TNF-alpha activates the transcription factor nuclear factor-kappaB, which in turn promotes transcription of many genes, including cyclooxygenase-2 (COX-2). COX-2 is in the brain and is an enzyme responsible for production of prostaglandin D-2. The hypothesis that central COX-2 plays a role in the regulation of spontaneous and TNF-alpha-induced sleep was investigated. Three doses (0.5, 5, and 50 mug) of NS-398, a highly selective COX-2 inhibitor, were injected intracerebroventricularly. The highest dose decreased non-rapid eye movement sleep. The intermediate and highest doses decreased electroencephalographic slow-wave activity; the greatest reduction occurred after 50 mug of NS-398 during the first 3-h postinjection period. Rapid eye movement sleep and brain temperature were not altered by any dose of NS-398. Pretreatment of rabbits with 5 or 50 mug of NS-398 blocked the TNF-alpha-induced increases in non-rapid eye movement sleep, electroencephalographic slow-wave activity, and brain temperature. These data suggest that COX-2 is involved in the regulation of spontaneous and TNF-alpha-induced sleep.
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