Repeated sleep restriction in rats leads to homeostatic and allostatic responses during recovery sleep
Repeated sleep restriction in rats leads to homeostatic and allostatic responses during recovery sleep
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DOI：
10.1073/pnas.0610351104
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发表时间：
2007-06-19
影响因子：
11.1
通讯作者：
Turek, Fred W.
中科院分区：
文献类型：
--
作者：
Kim, Youngsoo;Laposky, Aaron D.;Turek, Fred W.
最近的研究表明，慢性睡眠限制可能对大脑功能和外周生理产生负面影响，并可能导致全身的非稳态负荷。有趣的是，很少有研究探讨睡眠-觉醒系统本身如何对反复的睡眠限制做出反应。在这项研究中，大鼠进行了睡眠限制协议，包括20小时的睡眠剥夺（SD），然后是4小时的睡眠机会，每天连续5天。响应于第1天的第一个20小时SD阻断，动物在4小时睡眠机会期间以增强的睡眠强度响应[即，与基线相比，非快速眼动（NREM）δ功率]和快速眼动睡眠时间增加。这种睡眠模式表明了对急性睡眠不足的自我平衡反应。值得注意的是，在第2 - 5天的20小时SD阻断后，动物在4小时睡眠机会期间未能表现出补偿性NREM δ功率响应，并且未能增加NREM和快速眼动睡眠时间，尽管连续每天积累睡眠债。在5天的睡眠限制中失去了大约35小时的睡眠后，动物几乎没有恢复他们失去的睡眠，即使在整整3天的恢复期内。这些数据表明，补偿/稳态睡眠反应急性SD不推广到慢性部分睡眠丧失的条件。我们建议，在反复睡眠限制的背景下，睡眠-觉醒调节的变化反映了一个非稳态过程，由SD产生的非稳态负荷对睡眠-觉醒调节系统有直接影响。
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 approximate 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.