Repeated sleep restriction in rats leads to homeostatic and allostatic responses during recovery sleep

• Published in: Proceedings of the National Academy of Sciences - PNAS Vol. 104; no. 25; pp. 10697 - 10702
• Main Authors: Kim, Youngsoo, Laposky, Aaron D, Bergmann, Bernard M, Turek, Fred W
• Format: Journal Article
• Language: English
• Published: United States National Academy of Sciences 19-06-2007; National Acad Sciences
• Subjects: Allostasis; Allostasis - physiology; Animal behavior; Animals; Biological Sciences; Chronic Disease; Electroencephalography; Eye movements; Homeostasis; Insomnia; Male; Physiological regulation; Rapid eye movement sleep; Rats; Rats, Inbred F344; Rodents; Sleep; Sleep - physiology; Sleep deprivation; Sleep Deprivation - physiopathology; Wakefulness
• ISSN: 0027-8424; 1091-6490
• DOI: 10.1073/pnas.0610351104

Recent studies indicate that chronic sleep restriction can have negative consequences for brain function and peripheral physiology and can contribute to the allostatic load throughout the body. Interestingly, few studies have examined how the sleep-wake system itself responds to repeated sleep restriction. In this study, rats were subjected to a sleep-restriction protocol consisting of 20 h of sleep deprivation (SD) followed by a 4-h sleep opportunity each day for 5 consecutive days. In response to the first 20-h SD block on day 1, animals responded during the 4-h sleep opportunity with enhanced sleep intensity [i.e., nonrapid eye movement (NREM) delta power] and increased rapid eye movement sleep time compared with baseline. This sleep pattern is indicative of a homeostatic response to acute sleep loss. Remarkably, after the 20-h SD blocks on days 2-5, animals failed to exhibit a compensatory NREM delta power response during the 4-h sleep opportunities and failed to increase NREM and rapid eye movement sleep times, despite accumulating a sleep debt each consecutive day. After losing [almost equal to]35 h of sleep over 5 days of sleep restriction, animals regained virtually none of their lost sleep, even during a full 3-day recovery period. These data demonstrate that the compensatory/homeostatic sleep response to acute SD does not generalize to conditions of chronic partial sleep loss. We propose that the change in sleep-wake regulation in the context of repeated sleep restriction reflects an allostatic process, and that the allostatic load produced by SD has direct effects on the sleep-wake regulatory system.