β oscillation during slow wave sleep and rapid eye movement sleep in the electroencephalogram of a transgenic mouse model of Huntington's disease.

β oscillation during slow wave sleep and rapid eye movement sleep in the electroencephalogram of a transgenic mouse model of Huntington's disease.
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DOI:
10.1371/journal.pone.0079509
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发表时间:
2013
期刊:
影响因子:
3.7
通讯作者:
Cho YH
Cho YH
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Jeantet Y;Cayzac S;Cho YH

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在遗传性神经退行性亨廷顿病(HD)转基因小鼠模型中寻找可能先于运动症状的睡眠期脑电图(EEG)早期异常。在HD的R6/1转基因小鼠模型中,通过疾病的发作和进展纵向监测EEG记录中的节律性脑活动,并跨越警戒状态。从9-11周(症状前期)开始到6-7个月(症状期),在唤醒-睡眠周期(4小时)内每月记录植入慢性电极的小鼠。记录数据揭示了一种独特的β节律(20-35 Hz),仅存在于R6/1转基因小鼠中,其与疾病的发展密切平行。此外,这种β振荡和警觉状态之间存在着一种不寻常的关系:虽然在活跃的清醒状态下几乎不存在,但β振荡出现在困倦和慢波睡眠(SWS)期间,有趣的是,当大脑在快速眼动(REM)睡眠期间恢复到激活状态时,β振荡会加强而不是消失。除了提供一种新的体内生物标志物和对亨廷顿病病理生理学的深入了解外,这种偶然的观察为SWS和REM睡眠期间皮质基底神经节回路的神经生理学研究打开了一扇窗。
To search for early abnormalities in electroencephalogram (EEG) during sleep which may precede motor symptoms in a transgenic mouse model of hereditary neurodegenerative Huntington’s disease (HD). In the R6/1 transgenic mouse model of HD, rhythmic brain activity in EEG recordings was monitored longitudinally and across vigilance states through the onset and progression of disease. Mice with chronic electrode implants were recorded monthly over wake-sleep cycles (4 hours), beginning at 9–11 weeks (presymptomatic period) through 6–7 months (symptomatic period). Recording data revealed a unique β rhythm (20–35 Hz), present only in R6/1 transgenic mice, which evolves in close parallel with the disease. In addition, there was an unusual relationship between this β oscillation and vigilance states: while nearly absent during the active waking state, the β oscillation appeared with drowsiness and during slow wave sleep (SWS) and, interestingly, strengthened rather than dissipating when the brain returned to an activated state during rapid eye movement (REM) sleep. In addition to providing a new in vivo biomarker and insight into Huntington's disease pathophysiology, this serendipitous observation opens a window onto the rarely explored neurophysiology of the cortico-basal ganglia circuit during SWS and REM sleep.
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