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Am J Physiol Regul Integr Comp Physiol (April 28, 2005). doi:10.1152/ajpregu.00093.2005
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Submitted on February 10, 2005
Accepted on April 26, 2005

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

F. C Baker1, C. Angara2, R. Szymusiak3, and D. McGinty4*

1 Psychology, University of California, Los Angeles, CA, USA; Brain Function Research Unit, School of Physiology, University of the Witwatersrand, Johannesburg, South Africa
2 Psychology, University of California, Los Angeles, CA, USA
3 Medicine, University of California, Los Angeles, CA, USA; Research Service, V. A. Greater Los Angeles Healthcare System, North Hills, CA, USA
4 Psychology, University of California, Los Angeles, CA, USA; Research Service, V. A. Greater Los Angeles Healthcare System, North Hills, CA, USA

* To whom correspondence should be addressed. E-mail: dmcginty{at}ucla.edu.

The suprachiasmatic nucleus (SCN) regulates the circadian rhythms of body temperature (Tb) and vigilance states in mammals. We studied rats in which circadian rhythmicity was abolished after SCN lesions, to investigate the association between the ultradian rhythms of sleep-wake states and brain temperature (Tbr), which are exposed after lesions. An ultradian rhythm of Tbr (mean period = 3.6 h) and sleep were closely associated in SCNx rats. This association was also apparent in sham lesioned controls. Within each ultradian cycle, non-rapid eye movement (NREM) sleep was initiated 5 ± 1 min after Tbr peaks, after which temperature continued a slow decline (0.02 ± 0.006 °C/min) until reaching a minimum. Sleep and slow wave activity (SWA), an index of sleep intensity, were associated with declining temperature. Cross-correlation analysis also revealed that the rhythm of Tbr preceded that of SWA by 2-10 min. These results suggest that a drop in Tbr may signal sleep onset. 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 Tbr, blunted the amplitude of ultradian Tbr rhythms, and increased the number of transitions into NREM sleep, but did not significantly affect NREM sleep or SWA. Finally, SCNx rats and controls had a similar percentage of NREM sleep, REM sleep and wake as well as the same average Tb 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 body temperature during deviations in ambient temperature.







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