Edgar D M, Dement W C, Fuller C A
Department of Animal Physiology, University of California, Davis 95616.
J Neurosci. 1993 Mar;13(3):1065-79. doi: 10.1523/JNEUROSCI.13-03-01065.1993.
Sleep and wakefulness are governed by both the suprachiasmatic nuclei of the hypothalamus (SCN), and a sleep homeostatic process; however, the interaction of these control systems is not well understood. From rodent studies it has been assumed that the SCN promote neither wake nor sleep but gate the homeostatic sleep-promoting process. Yet in humans sleep tendency is lowest during the later waking hours of the day, and sleep duration can be predicted because of the precise circadian timing of waking. Thus in primates, the SCN could assure sleep-wake cycle consolidation by actively promoting or facilitating wakefulness. To evaluate this hypothesis, we examined the sleep-wake and sleep-stage patterns of intact and SCN-lesioned (SCNx) squirrel monkeys maintained in constant light. This diurnal primate has consolidated sleep and wake patterns more similar to man than rodents. Sleep-wake, sleep stages, brain temperature, and drinking circadian rhythms were eliminated, and total sleep time was significantly increased (4.0 hr, P < 0.01) in SCNx monkeys. However, total times in deeper stages of non-rapid eye movement (non-REM; e.g., delta sleep) and REM sleep were not significantly affected by SCN lesions. Increased total sleep time was associated with a reduction in subjective day wake consolidation, as evidenced by substantially shorter wake bout lengths in SCNx monkeys (15 +/- 6 min) as compared to intact monkeys (223 +/- 10 min; P < 0.0001, ANOVA). These findings show that the SCN influence the regulation of daily total wake and sleep times, and implicate an alternative sleep-wake regulatory model in which an SCN-dependent process actively facilitates the initiation and maintenance of wakefulness and opposes homeostatic sleep tendency during the subjective day in diurnal primates.
睡眠和觉醒受下丘脑视交叉上核（SCN）以及睡眠稳态过程的共同调控；然而，这些控制系统之间的相互作用尚未完全明晰。从啮齿动物研究中可以推测，SCN既不促进觉醒也不促进睡眠，而是为稳态睡眠促进过程提供“闸门”。然而在人类中，一天中较晚的清醒时段睡眠倾向最低，并且由于清醒时间的精确昼夜节律，睡眠时间是可以预测的。因此，在灵长类动物中，SCN可能通过积极促进或推动觉醒，来确保睡眠 - 觉醒周期的巩固。为了评估这一假设，我们研究了饲养在持续光照环境下的完整和SCN损伤（SCNx）松鼠猴的睡眠 - 觉醒及睡眠阶段模式。这种昼行性灵长类动物的睡眠和觉醒模式比啮齿动物更接近人类。SCNx猴子的睡眠 - 觉醒、睡眠阶段、脑温及饮水昼夜节律均被消除，总睡眠时间显著增加（4.0小时，P < 0.01）。然而，非快速眼动（non-REM；例如，δ睡眠）和快速眼动睡眠的较深阶段的总时长并未受到SCN损伤的显著影响。总睡眠时间的增加与主观日觉醒巩固的减少相关，这表现为SCNx猴子的清醒时段长度（15±6分钟）显著短于完整猴子（223±10分钟；P < 0.0001，方差分析）。这些发现表明，SCN影响每日总觉醒和睡眠时间的调节，并暗示了一种替代的睡眠 - 觉醒调节模型，即在昼行性灵长类动物的主观日期间，一个依赖SCN的过程积极促进觉醒的起始和维持，并对抗稳态睡眠倾向。
