完全睡眠剥夺后,ARC基因型调节慢波睡眠和睡眠脑电图频谱功率。

Brieann C Satterfield, Myles G Finlay, Sofia K Fluke, Lillian Skeiky, Michelle A Schmidt, Jonathan P Wisor, Hans P A Van Dongen
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引用次数: 0

摘要

研究目的:睡眠剥夺的稳态反应存在很大的个体差异,这反映在慢波睡眠(SWS)和脑电图(EEG)频谱功率上,这在很大程度上尚未得到解释。最近的证据表明可能与活性调控的细胞骨架相关蛋白(ARC)基因有关。在这里,我们评估了人类ARC基因(rs35900184)的“c.*742 + 58C > T非编码单核苷酸多态性”对完全睡眠剥夺(TSD)时睡眠-生理和清醒-神经行为反应的影响。方法:50名健康的年轻人参加了一项为期4天/3夜的实验室研究,其中有38小时的创伤后应激障碍期,同时有10小时的基线和恢复睡眠机会。采用多导睡眠仪记录睡眠,并对非快速眼动(NREM)和快速眼动(REM)睡眠的脑电图进行波谱分析。采用精神运动警觉性测验(PVT)和卡罗林斯卡嗜睡量表(KSS)测量清醒时的神经行为功能。结果:与T等位基因携带者相比,ARC C/C纯合子在ptsd后恢复性睡眠中表现出更大的SWS反弹。ARC T/T纯合子在NREM theta和alpha波段以及REM delta、theta、alpha和beta波段的脑电图频谱功率均增加,但在NREM delta功率对TSD的反应中没有显著的基因型差异。TSD对PVT表现和KSS嗜睡的影响也没有显著的基因型差异。结论:ARC基因型影响创伤后睡眠生理反弹的个体差异。然而,我们的研究结果仅与ARC介导睡眠剥夺的睡眠稳态反应部分一致。这篇文章是睡眠、睡眠障碍和昼夜节律的遗传和其他分子基础的一部分,包括翻译方法集合。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

<i>ARC</i> genotype modulates slow wave sleep and spectral power in the sleep EEG after total sleep deprivation.

<i>ARC</i> genotype modulates slow wave sleep and spectral power in the sleep EEG after total sleep deprivation.

<i>ARC</i> genotype modulates slow wave sleep and spectral power in the sleep EEG after total sleep deprivation.

ARC genotype modulates slow wave sleep and spectral power in the sleep EEG after total sleep deprivation.

Study objectives: There are large individual differences in the homeostatic response to sleep deprivation, as reflected in slow wave sleep (SWS) and electroencephalogram (EEG) spectral power, which have largely been left unexplained. Recent evidence suggests the possible involvement of the activity-regulated cytoskeleton-associated protein (ARC) gene. Here we assessed the effects of the "c.*742 + 58C > T non-coding single nucleotide polymorphism" of the human ARC gene (rs35900184) on sleep-physiological and waking-neurobehavioral responses to total sleep deprivation (TSD).

Methods: N = 50 healthy, young adults participated in a 4-day/3-night in-laboratory study with a 38-h TSD period, flanked by 10-h baseline and recovery sleep opportunities. Sleep was recorded polysomnographically and the EEG of non-rapid eye movement (NREM) and rapid eye movement (REM) sleep was subjected to spectral analysis. Waking neurobehavioral functioning was measured with the psychomotor vigilance test (PVT) and the Karolinska Sleepiness Scale (KSS).

Results: ARC C/C homozygotes, compared to T allele carriers, showed a greater SWS rebound during recovery sleep after TSD relative to baseline. ARC T/T homozygotes showed increased EEG spectral power in the NREM theta and alpha bands and in the REM delta, theta, alpha, and beta bands, but there was no significant genotype difference in the NREM delta power response to TSD. There were also no significant genotype differences in the impact of TSD on PVT performance and KSS sleepiness.

Conclusions: Individual differences in the sleep physiological rebound after TSD were influenced by ARC genotype. However, our findings were only partially consistent with ARC mediating the sleep homeostatic response to sleep deprivation. This article is part of the Genetic and Other Molecular Underpinnings of Sleep, Sleep Disorders, and Circadian Rhythms Including Translational Approaches Collection.

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