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1 Department of Veterinary and Comparative Anatomy, Pharmacology, and Physiology, Washington State University College of Veterinary Medicine, Pullman, Washington 99164-6520; and 2 Department of Biological Science, Fordham University, Bronx, New York 10458
Both tumor
necrosis factor (TNF) and interleukin (IL)-1 are somnogenic cytokines.
They also induce each other's production and both induce nuclear
factor kappa B activation, which in turn enhances IL-1 and TNF
transcription. We hypothesized that TNF and IL-1 could influence each
other's somnogenic actions. To test this hypothesis, we determined the
effects of blocking both endogenous TNF and IL-1 on spontaneous sleep
and on sleep rebound after sleep deprivation in rabbits. Furthermore,
the effects of inhibition of TNF on IL-1-induced sleep and the effects
of blocking IL-1 on TNF-induced sleep were determined. A TNF receptor
fragment (TNFRF), as a TNF inhibitor, and an IL-1 receptor fragment
(IL-1RF), as an IL-1 inhibitor, were used. Intracerebroventricular
injection of a combination of the TNFRF plus the IL-1RF significantly
reduced spontaneous non-rapid eye movement sleep by 87 min over a 22-h recording period. Pretreatment of rabbits with the combination of TNFRF
and IL-1RF also significantly attenuated sleep rebound after sleep
deprivation. Furthermore, the TNFRF significantly attenuated
IL-1-induced sleep but not fever. Finally, the IL-1RF blocked
TNF-induced sleep responses but not fever. Results indicate that TNF
and IL-1 cooperate to regulate physiological sleep.
cytokine; fever; electroencephalogram; rabbit
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