Recovery Sleep Following Sleep Deprivation in Intact and Suprachiasmatic Nuclei-Lesioned Rats
Author(s) -
Ralph E. Mistlberger,
Bernard M. Bergmann,
William Waldenar,
Allan Rechtschaffen
Publication year - 1983
Publication title -
sleep
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.222
H-Index - 207
eISSN - 1550-9109
pISSN - 0161-8105
DOI - 10.1093/sleep/6.3.217
Subject(s) - non rapid eye movement sleep , circadian rhythm , sleep (system call) , endocrinology , free running sleep , medicine , sleep deprivation , slow wave sleep , rapid eye movement sleep , suprachiasmatic nucleus , psychology , anesthesia , neuroscience , electroencephalography , light effects on circadian rhythm , computer science , operating system
Recovery sleep was studied for 3-5 days following 24 h of sleep deprivation (TSD) in normal rats and in rats lacking circadian rhythms (CRs) of sleep because of prior lesioning of the suprachiasmatic nuclei (SCN). One group of lesioned rats was run in constant dim light. Another lesioned group and an intact group were run on a 12:12 dark-light schedule with TSD and recovery beginning at lights-off. All groups showed immediate rebounds of high-amplitude NREM sleep and paradoxical sleep, confined mostly to the first 12-18 h of recovery, and decreases in moderate and low-amplitude NREM sleep during the first 6-12 h of recovery. Thus, sleep stage rebound priorities were little affected by CRs. Total sleep rebound was initially greatest in intact rats, but limited mostly to the first 12 h of recovery. Total sleep rebound was distributed over a longer period in SCN rats, but total accumulated rebound was similar in all groups. Thus, CRs appear to modulate the timing but not the amount of accumulated total sleep rebound. Results were interpreted in terms of ceiling effects on total sleep, delayed rebounds, and competition between CRs and homeostatic recovery processes. Recovery sleep of lesioned rats on the dark-light schedule was marked by a transient diurnal rhythm.
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