Persistence of sleep-temperature coupling after suprachiasmatic nuclei lesions in rats

Abstract

The suprachiasmatic nucleus (SCN) regulates the circadian rhythms of body temperature (T_b) and vigilance states in mammals. We studied rats in which circadian rhythmicity was abolished after SCN lesions (SCNx rats) to investigate the association between the ultradian rhythms of sleep-wake states and brain temperature (T_br), which are exposed after lesions. Ultradian rhythms of T_br (mean period: 3.6 h) and sleep were closely associated in SCNx rats. Within each ultradian cycle, nonrapid eye movement (NREM) sleep was initiated 5 ± 1 min after T_br peaks, after which temperature continued a slow decline (0.02 ± 0.006°C/min) until it reached a minimum. Sleep and slow wave activity (SWA), an index of sleep intensity, were associated with declining temperature. Cross-correlation analysis revealed that the rhythm of T_br preceded that of SWA by 2–10 min. We also investigated the thermoregulatory and sleep-wake responses of SCNx rats and controls to mild ambient cooling (18°C) and warming (30°C) over 24-h periods. SCNx rats and controls responded similarly to changes in ambient temperature. Cooling decreased REM sleep and increased wake. Warming increased T_br, blunted the amplitude of ultradian T_br rhythms, and increased the number of transitions into NREM sleep. SCNx rats and controls had similar percentages of NREM sleep, REM sleep, and wake, as well as the same average T_b within each 24-h period. Our results suggest that, in rats, the SCN modulates the timing but not the amount of sleep or the homeostatic control of sleep-wake states or T_b during deviations in ambient temperature.