Keeping cool: a hypothesis about the mechanisms and functions of slow-wave sleep.

Current evidence supports a hypothesis that slow-wave sleep (SWS) in mammals and birds is controlled by thermoregulatory mechanisms, and provides brain and body cooling as a primary homeostatic feedback process. Recent work has identified a medial preoptic area anterior hypothalamic and basal forebrain neuronal network which integrates thermoregulatory and hypnogenic controls. This network induces EEG and behavioral deactivation, in part, through suppression of the reticular activating system. Studies have shown that SWS, like other heat loss processes, is facilitated when brain temperature exceeds a threshold level. This threshold is hypothesized to be determined by responses of POAH thermosensitive neurons and to be regulated by both circadian and homeostatic processes. Many known chemomodulators of SWS appear to act on this hypnogenic thermoregulatory system. At a functional level, SWS-induced brain and body cooling would provide several adaptations including lower energy utilization, reduced cerebral metabolism, protection of the brain against the sustained high temperatures of wakefulness, facilitation of immune defense processes and regulation of the timing of behavioral activity relative to the circadian light-dark cycle. This concept provides a comprehensive model for analysis of sleep homeostasis.