Department of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI 48109-5622, USA.
Exp Neurol. 2011 Dec;232(2):168-75. doi: 10.1016/j.expneurol.2011.08.020. Epub 2011 Aug 30.
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 h 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.
睡眠障碍是中风的重要危险因素;相反,中风患者会出现睡眠障碍,包括非快速眼动(NREM)和快速眼动(REM)睡眠中断,以及总睡眠时间减少。本研究旨在使用连续脑电图(EEG)和活动监测来描述中风对大鼠睡眠结构的影响。大鼠被植入发射器,使其能够连续实时记录 EEG、肌电图(EMG)和运动活动。在诱导短暂性大脑中动脉(MCA)闭塞或假手术之前进行基线记录。手术后进行 60 小时的睡眠记录,以在中风前后识别清醒、NREM 和 REM 睡眠期。进行频谱分析以评估中风对状态相关 EEG 的影响。最后,我们量化了中风前后的清醒、NREM 和 REM 睡眠时间。中风后一天,δ功率(衡量 NREM 睡眠深度的指标)增加。与此同时,在 REM 和清醒期间,θ节律明显向较低频率转移。中风后,大脑两个半球的清醒 EEG 都变慢了。缺血半球的 EEG 显示,与对侧半球相比,θ功率明显减少,特别是 REM 减少。与接受假手术的大鼠相比,后者总睡眠时间略有增加,而经历中风的大鼠总睡眠时间减少。中风后总睡眠时间减少是由于缺血后 REM 睡眠时间的大幅减少所致。中风后 REM 抑制是由于 REM 发作次数减少所致;平均 REM 发作的长度没有变化。我们得出结论,在这个实验模型中,中风后大鼠的 REM 睡眠受到特别且严重的抑制。应使用该实验模型进行进一步实验,以研究中风后 REM 抑制的机制和后果。