Abstract
It is well established that cytokines such as tumor necrosis factor-α (TNFα) and interleukin-1β (IL-1β) are involved in physiological sleep regulation, yet their downstream somnogenic mechanisms remain largely uninvestigated. Nitric oxide (NO) is an effector molecule for some TNFα actions. Neuronal nitric oxide synthase (nNOS) and inducible nitric oxide synthase (iNOS) gene knockout (KO) mice sleep differently than their respective controls. In this study, we tested the hypothesis that NO mediates TNFα-induced sleep using iNOS and nNOS KO mice and their corresponding wild-type controls. Systemic administration of TNFα increased non-rapid eye movement sleep (NREMS) in the two control strains and in the iNOS KO mice during the first 4 h post-injection but failed to increase NREMS in nNOS KO mice. Rapid eye movement sleep (REMS) was suppressed by TNFα in nNOS controls but not in the other strains examined. The results suggest that TNFα affects sleep, in part, through nNOS.
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