Kim Youngsoo, Laposky Aaron D, Bergmann Bernard M, Turek Fred W
Center for Sleep and Circadian Biology, Department of Neurobiology and Physiology, Northwestern University, Evanston, IL 60208, USA.
Proc Natl Acad Sci U S A. 2007 Jun 19;104(25):10697-702. doi: 10.1073/pnas.0610351104. Epub 2007 Jun 4.
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 approximately 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.
最近的研究表明,长期睡眠受限会对脑功能和外周生理产生负面影响,并会增加全身的应激负荷。有趣的是,很少有研究探讨睡眠-觉醒系统本身如何应对反复的睡眠限制。在本研究中,大鼠接受了一种睡眠限制方案,即每天连续5天,先进行20小时的睡眠剥夺(SD),然后有4小时的睡眠机会。在第1天对首个20小时的SD时段做出反应时,与基线相比,动物在4小时的睡眠机会中表现出睡眠强度增强[即非快速眼动(NREM)δ波功率]以及快速眼动睡眠时间增加。这种睡眠模式表明对急性睡眠缺失存在稳态反应。值得注意的是,在第2 - 5天的20小时SD时段之后,尽管每天都积累了睡眠债,但动物在4小时的睡眠机会中未能表现出代偿性的NREM δ波功率反应,也未能增加NREM和快速眼动睡眠时间。在5天的睡眠限制中失去约35小时睡眠后,即使在整整3天的恢复期内,动物几乎没有恢复任何失去的睡眠。这些数据表明,对急性SD的代偿性/稳态睡眠反应并不适用于慢性部分睡眠缺失的情况。我们提出,在反复睡眠限制的背景下,睡眠-觉醒调节的变化反映了一种适应性变化过程,并且SD产生的应激负荷对睡眠-觉醒调节系统有直接影响。