Subdiaphragmatic vagotomy does not block sleep deprivation-induced sleep in rats.

Cytokines, such as interleukin-1beta (IL-1beta), are involved in physiological sleep regulation and in the sleep responses to sleep deprivation. Sleep deprivation increases systemic cytokine levels and recent evidence suggests that cytokine-to-brain communication occurs via the vagus nerve. Furthermore, the vagus nerve plays a role in sleep responses elicited by feeding and vagal activity affects electroencephalographic (EEG) activity. Thus, this study examined sleep-wake activity and brain temperature (Tbr) responses to sleep deprivation in subdiaphragmatically vagotomized and sham-operated rats. In control rats, 6 h of total sleep deprivation significantly increased nonrapid eye movement sleep (NREMS), rapid eye movement sleep (REMS), and electroencephalographic slow-wave activity during nonrapid eye movement sleep. Brain temperature was significantly increased during the 6 h of sleep deprivation and decreased following sleep deprivation. Vagotomy had no significant effects on any of these variables. These results indicate that the subdiaphragmatic vagus nerve is not critical in the sleep and thermoregulatory responses after 6 h of sleep deprivation. Together with other data, the current results suggest that central pools of interleukin-1 are important in moderate sleep deprivation-induced sleep responses and that vagotomy does not disrupt the ability to increase sleep using a well-known sleep-inducing stimulus likely mediated by brain cytokines.