The role of nitric oxide synthases in the sleep responses to tumor necrosis factor-alpha.
Brain Behav Immun
; 18(4): 390-8, 2004 Jul.
Article
em En
| MEDLINE
| ID: mdl-15157956
ABSTRACT
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) is an effector molecule for some TNFalpha 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 TNFalpha-induced sleep using iNOS and nNOS KO mice and their corresponding wild-type controls. Systemic administration of TNFalpha 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 TNFalpha in nNOS controls but not in the other strains examined. The results suggest that TNFalpha affects sleep, in part, through nNOS.
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Base de dados:
MEDLINE
Assunto principal:
Sono
/
Fator de Necrose Tumoral alfa
/
Óxido Nítrico Sintase
Limite:
Animals
Idioma:
En
Ano de publicação:
2004
Tipo de documento:
Article