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[用于转化研究的慢性睡眠限制建模]

[Modeling of chronic sleep restriction for translational studies].

作者信息

Guzeev M A, Kurmazov N S, Simonova V V, Pastukhov Yu F, Ekimova I V

机构信息

Sechenov Institute of Evolutionary Physiology and Biochemistry of the Russian Academy of Sciences, Saint Petersburg, Russia.

出版信息

Zh Nevrol Psikhiatr Im S S Korsakova. 2021;121(4. Vyp. 2):6-13. doi: 10.17116/jnevro20211214026.

Abstract

OBJECTIVE

To develop of a chronic sleep restriction model in rats by repeated sleep deprivation using an orbital shaker and to determine whether this model leads to disturbances in sleep homeostatic mechanisms.

MATERIAL AND METHODS

Male Wistar rats (7-8 months old) underwent sleep restriction for five consecutive days: 3 h of sleep deprivation and 1 h of sleep opportunity repeating throughout each day. Polysomnograms were recorded telemetrically throughout the day before sleep restriction (baseline), on the 1st, 3rd, 5th day of sleep restriction and 2 days after the end of sleep restriction (recovery period).

RESULTS

During the period of sleep restriction, the total amount of slow-wave sleep (SWS) and rapid eye movement (REM) sleep decreased by 61% and 55%, respectively, compared to baseline. On the first day of recovery, amount of SWS increased mainly in the dark (active) phase of the day, while REM sleep increased in both light and dark phases; there was no marked rebound of daily SWS amount, while REM sleep increased by 30% from baseline. On the first day of recovery, an elevation of EEG beta and sigma power in sleep states was observed mainly in the light phase of the day. The loss of deep SWS throughout the sleep restriction period increased from 50% on 1st day to 75% on 5th day. The level of deep SWS remained below the baseline by 15-20% on the two subsequent days of recovery. The findings suggest that homeostatic mechanisms of SWS are persistently impaired after 5-day chronic sleep restriction. Besides, a decline of wakefulness accompanied by an increase of SWS in the active phase of the recovery period indicates a disruption in circadian rhythm.

CONCLUSION

The proposed model leads to the disruption of sleep homeostatic mechanisms, which, in turn, impede compensation of SWS loss caused by chronic insufficient sleep.

摘要

目的

通过使用轨道振荡器反复剥夺睡眠来建立大鼠慢性睡眠限制模型,并确定该模型是否会导致睡眠稳态机制紊乱。

材料与方法

雄性Wistar大鼠(7 - 8个月大)连续五天进行睡眠限制:每天重复3小时睡眠剥夺和1小时睡眠机会。在睡眠限制前一天(基线)、睡眠限制的第1、3、5天以及睡眠限制结束后2天(恢复期)全天通过遥测记录多导睡眠图。

结果

在睡眠限制期间,与基线相比,慢波睡眠(SWS)和快速眼动(REM)睡眠总量分别减少了61%和55%。在恢复的第一天,SWS量主要在白天的黑暗(活跃)阶段增加,而REM睡眠在白天的光明和黑暗阶段均增加;每日SWS量没有明显反弹,而REM睡眠比基线增加了30%。在恢复的第一天,主要在白天的光明阶段观察到睡眠状态下脑电图β和σ功率升高。在整个睡眠限制期间,深度SWS的损失从第一天的50%增加到第五天的75%。在恢复的随后两天,深度SWS水平比基线低15 - 20%。这些发现表明,5天慢性睡眠限制后SWS的稳态机制持续受损。此外,恢复期活跃阶段清醒度下降并伴有SWS增加表明昼夜节律紊乱。

结论

所提出的模型导致睡眠稳态机制破坏,进而阻碍对慢性睡眠不足引起的SWS损失的补偿。

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