作者: Lichao Chen , Ping Taishi , Jeannine A. Majde , Zoltan Peterfi , Ferenc Obal
DOI: 10.1016/J.BBI.2003.12.002
关键词:
摘要: It is well established that cytokines such as tumor necrosis factor-alpha (TNFalpha) and interleukin-1beta (IL-1beta) are involved in physiological sleep regulation, yet their downstream somnogenic mechanisms remain largely uninvestigated. Nitric oxide (NO) an effector molecule for some TNFalpha actions. Neuronal nitric synthase (nNOS) inducible (iNOS) gene knockout (KO) mice differently than respective controls. In this study, we tested the hypothesis NO mediates TNFalpha-induced using iNOS nNOS KO corresponding wild-type Systemic administration of increased non-rapid eye movement (NREMS) two control strains during first 4 h post-injection but failed to increase NREMS mice. Rapid (REMS) was suppressed by controls not other examined. The results suggest affects sleep, part, through nNOS.