Context: Sleep is regulated by circadian and homeostatic processes. The circadian pacemaker, located in the suprachiasmatic nuclei (SCN), regulates the timing and consolidation of the sleep-wake cycle, while a homeostatic mechanism governs the accumulation of sleep debt and sleep recovery. Recent studies using mice with deletions or mutations of circadian genes show that components of the circadian pacemaker can influence the total amount of baseline sleep and recovery from sleep deprivation, indicating a broader role for the SCN in sleep regulation. Objective: To further investigate the role of the circadian pacemaker in sleep regulation in mice, we recorded sleep in sham and SCN-lesioned mice under baseline conditions and following sleep deprivation. Results: Compared to sham controls, SCN-lesioned mice exhibited a decrease in sleep consolidation and a decrease in wakefulness during the dark phase. Following sleep deprivation, SCN-lesioned mice exhibited an attenuated increase in non-rapid eye movement sleep time but an increase in non-rapid eye movement sleep electroencephalographic delta power that was similar to that of the sham controls. Conclusions: These findings support the hypothesis that the SCN consolidate the sleep-wake cycle by generating a signal of arousal during the subjective night (ie. the active period), thereby having the capacity to alter baseline sleep amount. Although the SCN are not involved in sleep homeostasis as defined by the increase in electroencephalographic delta power after sleep deprivation, the SCN does play a central role in the regulation of sleep and wakefulness beyond just the timing of vigilance states.
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