Study objectives: In mammals, sleep is controlled by a homeostatic process, which regulates depth of sleep, and by the circadian clock of the suprachiasmatic nucleus (SCN), which regulates 24-h rhythms in timing of sleep. Sleep deprivation is known to cause molecular and physiological changes and results in an alteration in the timing of sleep. It is generally assumed that following sleep deprivation, homeostatic mechanisms overrule the circadian clock, allowing animals to sleep during their active phase. However, recent evidence indicates that sleep states have direct access to the circadian pacemaker of the SCN. We questioned therefore whether sleep deprivation may have long-term effects on the circadian pacemaker, which may explain altered sleep patterns following sleep deprivation.
Design: To test this hypothesis, we combined SCN recordings of electrical impulse frequency through stationary implanted electrodes in freely moving rats with electroencephalogram recordings in the same animal before, during, and after a mild 6-h sleep deprivation.
Measurements and results: Following sleep deprivation, SCN neuronal activity was significantly reduced to about 60% of baseline levels. The decrements in SCN activity were most obvious during NREM sleep and REM sleep and lasted for 6-7 hours.
Conclusions: The data show that sleep deprivation influences not only sleep homeostatic mechanisms, but also SCN electrical activity, resulting in a strong reduction in circadian amplitude in the major output signal from the SCN.