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纳曲酮和巴氯芬对脑电图、睡眠、神经行为表现和记忆的影响差异。

Differential effects of sodium oxybate and baclofen on EEG, sleep, neurobehavioral performance, and memory.

机构信息

Center for Integrative Genomics (CIG), University of Lausanne, Lausanne, Switzerland.

出版信息

Sleep. 2012 Aug 1;35(8):1071-83. doi: 10.5665/sleep.1992.

Abstract

STUDY OBJECTIVES

Sodium oxybate (SO) is a GABAβ agonist used to treat the sleep disorder narcolepsy. SO was shown to increase slow wave sleep (SWS) and EEG delta power (0.75-4.5 Hz), both indexes of NREM sleep (NREMS) intensity and depth, suggesting that SO enhances recuperative function of NREM. We investigated whether SO induces physiological deep sleep.

DESIGN

SO was administered before an afternoon nap or before the subsequent experimental night in 13 healthy volunteers. The effects of SO were compared to baclofen (BAC), another GABAβ receptor agonist, to assess the role of GABAβ receptors in the SO response.

MEASUREMENTS AND RESULTS

As expected, a nap significantly decreased sleep need and intensity the subsequent night. Both drugs reversed this nap effect on the subsequent night by decreasing sleep latency and increasing total sleep time, SWS during the first NREMS episode, and EEG delta and theta (0.75-7.25 Hz) power during NREMS. The SO-induced increase in EEG delta and theta power was, however, not specific to NREMS and was also observed during REM sleep (REMS) and wakefulness. Moreover, the high levels of delta power during a nap following SO administration did not affect delta power the following night. SO and BAC taken before the nap did not improve subsequent psychomotor performance and subjective alertness, or memory consolidation. Finally, SO and BAC strongly promoted the appearance of sleep onset REM periods.

CONCLUSIONS

The SO-induced EEG slow waves seem not to be functionally similar to physiological slow waves. Our findings also suggest a role for GABAβ receptors in REMS generation.

摘要

研究目的

羟丁酸钠(SO)是一种 GABAβ 激动剂,用于治疗睡眠障碍性发作性睡病。SO 被证明可增加慢波睡眠(SWS)和 EEG 德尔塔功率(0.75-4.5 Hz),这两个指标均为非快速眼动睡眠(NREMS)强度和深度的指标,这表明 SO 增强了 NREMS 的恢复功能。我们研究了 SO 是否诱导生理性深度睡眠。

设计

SO 在 13 名健康志愿者下午小睡前或随后的实验夜前给药。将 SO 的作用与另一种 GABAβ 受体激动剂巴氯芬(BAC)进行比较,以评估 GABAβ 受体在 SO 反应中的作用。

测量和结果

正如预期的那样,小睡显著降低了随后夜晚的睡眠需求和强度。两种药物均通过降低睡眠潜伏期和增加总睡眠时间、第一个 NREMS 发作期间的 SWS 以及 NREMS 期间的 EEG 德尔塔和θ(0.75-7.25 Hz)功率,逆转了小睡对随后夜晚的影响。然而,SO 诱导的 EEG 德尔塔和θ功率增加并不是 NREMS 特异性的,也观察到在 REM 睡眠(REMS)和清醒状态下。此外,SO 给药后小睡期间的高 delta 功率水平不会影响随后夜晚的 delta 功率。SO 和 BAC 在小睡前服用并不能改善随后的运动表现和主观警觉性或记忆巩固。最后,SO 和 BAC 强烈促进了睡眠开始 REM 期的出现。

结论

SO 诱导的 EEG 慢波似乎在功能上与生理性慢波不同。我们的研究结果还表明 GABAβ 受体在 REMS 产生中起作用。

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