Ischemic stroke selectively inhibits REM sleep of rats.

Ischemic stroke selectively inhibits REM sleep of rats.
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DOI:
10.1016/j.expneurol.2011.08.020
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发表时间:
2011-12
影响因子:
5.3
通讯作者:
Wang, Michael M.
Wang, Michael M.
中科院分区:
医学2区
文献类型:
--
作者:
Ahmed, Samreen;Meng, He;Liu, Tiecheng;Sutton, Blair C.;Opp, Mark R.;Borjigin, Jimo;Wang, Michael M.

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睡眠障碍是中风的重要风险因素;相反,中风患者会受到睡眠障碍的困扰,包括非快速眼动(NREM)和快速眼动(REM)睡眠中断以及总睡眠减少。本研究采用连续脑电(EEG)和活动监测的方法,研究了中风对大鼠睡眠结构的影响。在大鼠体内植入发射器,使其能够连续实时记录脑电、肌电(EMG)和运动活动。基线记录在大脑中动脉(MCA)暂时性闭塞或假手术诱导前进行。获得手术后60小时的睡眠记录,以确定中风前和中风后的清醒、NREM和REM睡眠时间。频谱分析用于评估中风对状态依赖脑电的影响。最后,我们量化了中风前后觉醒、非快速眼动和快速眼动睡眠的时间。衡量NREM睡眠深度的Delta功率在中风后第二天就增加了。与此同时,在REM和觉醒期间,theta节律显著地向较低频率移动。在两个半球中风后,清醒的脑电波减慢。缺血半球的脑电显示,REM特有的theta能力减弱,超过对侧大脑半球的减慢。与接受假手术的大鼠相比,接受假手术的大鼠总睡眠略有增加,而中风大鼠的总睡眠减少。中风后总睡眠的减少是缺血后快速眼动睡眠急剧减少的结果。卒中后REM的抑制是由于REM发作次数的减少,平均REM发作的长度没有改变。我们得出结论,在这个实验模型中,中风后,大鼠的快速眼动睡眠受到特异性和深刻的抑制。使用这个实验模型的进一步实验应该被用来研究中风后快速眼动抑制的机制和后果。
Sleep disorders are important risk factors for stroke; conversely, stroke patients suffer from sleep disturbances including disruptions of non-rapid eye movement (NREM) and rapid eye movement (REM) sleep and a decrease in total sleep. This study was performed to characterize the effect of stroke on sleep architecture of rats using continuous electroencephalography (EEG) and activity monitoring. Rats were implanted with transmitters which enabled continuous real time recording of EEG, electromyography (EMG), and locomotor activity. Baseline recordings were performed prior to induction of either transient middle cerebral artery (MCA) occlusion or sham surgery. Sleep recordings were obtained for 60 hours after surgery to identify periods of wakefulness, NREM, and REM sleep before and after stroke. Spectral analysis was performed to assess the effects of stroke on state-dependent EEG. Finally, we quantified the time in wake, NREM, and REM sleep before and after stroke. Delta power, a measure of NREM sleep depth, was increased the day following stroke. At the same time, there was a significant shift in theta rhythms to a lower frequency during REM and wake periods. The awake EEG slowed after stroke over both hemispheres. The EEG of the ischemic hemisphere demonstrated diminished theta power specific to REM in excess of the slowing seen over the contralateral hemisphere. In contrast to rats exposed to sham surgery which had slightly increased total sleep, rats undergoing stroke experienced decreased total sleep. The decrease in total sleep after stroke was the result of dramatic reduction in the amount of REM sleep after ischemia. The suppression of REM after stroke was due to a decrease in the number of REM bouts; the length of the average REM bout did not change. We conclude that after stroke in this experimental model, REM sleep of rats is specifically and profoundly suppressed. Further experiments using this experimental model should be performed to investigate the mechanisms and consequences of REM suppression after stroke.
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