Alcohol disrupts sleep homeostasis.

Alcohol disrupts sleep homeostasis.
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酒精破坏了睡眠体内平衡。

DOI:
10.1016/j.alcohol.2014.07.019
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发表时间:
2015-06
期刊:
影响因子:
2.3
通讯作者:
Sahota, Pradeep
Sahota, Pradeep
中科院分区:
医学4区
文献类型:
--
作者:
Thakkar, Mahesh M.;Sharma, Rishi;Sahota, Pradeep

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酒精是一种有效的安眠药,也是最常用的“非处方”助眠药之一。在健康的非酗酒者中,急性酒精减少了睡眠潜伏期,巩固和增加了前半夜NREM睡眠的质量(δ功率)和数量。然而,睡眠在下半场被打断。酗酒者,无论是在饮酒期间还是在戒酒期间,都会遭受大量的睡眠中断,表现为严重的失眠,白天过度嗜睡和睡眠结构的改变。此外,睡眠障碍的主观和客观指标是复发的预测因子。最后,在美国,据估计,与酒精有关的睡眠障碍的社会成本超过180亿美元。因此,尽管酒精相关的睡眠问题具有显著的经济和临床后果,但人们对酒精如何以及在何处影响睡眠知之甚少。在这篇综述中,我们描述了我们试图了解酒精如何以及在何处影响睡眠。我们使用两种不同物种(大鼠和小鼠)作为动物模型,并结合多学科实验方法进行了一系列实验,以检查和了解介导急性和慢性酒精暴露对睡眠影响的解剖和细胞基质。觉醒。我们的研究结果表明,酒精的睡眠促进作用可能是通过酒精对睡眠稳态介质的作用来介导的:腺苷(AD)和基底前脑(BF)的促醒胆碱能神经元。酒精通过其对AD摄取的作用,增加细胞外AD,导致BF促醒神经元的抑制。损伤BF胆碱能神经元或阻断AD A1受体可减弱酒精诱导的睡眠促进作用,提示AD和BF胆碱能神经元对酒精的睡眠促进作用至关重要。由于酗酒是一种非常普遍的饮酒模式,并且会扰乱睡眠,因此我们研究了酗酒对睡眠觉醒的影响。我们的研究结果表明,睡眠稳态的破坏可能是酗酒后观察到的睡眠中断的主要原因。最后,我们还表明,在急性戒断期间观察到的失眠和相关的睡眠中断是由于睡眠稳态受损引起的。根据我们的研究结果,我们认为酒精可能会破坏睡眠稳态,导致睡眠中断。
Alcohol is a potent somnogen and one of the most commonly used “over the counter” sleep aids. In healthy non-alcoholics, acute alcohol decreases sleep latency, consolidates and increases the quality (delta power) and quantity of NREM sleep during the first half of the night. However, sleep is disrupted during the second half. Alcoholics, both during drinking periods and during abstinences, suffer from a multitude of sleep disruptions manifested by profound insomnia, excessive daytime sleepiness, and altered sleep architecture. Furthermore, subjective and objective indicators of sleep disturbances are predictors of relapse. Finally, within the USA, it is estimated that societal costs of alcohol-related sleep disorders exceeds $18 billion. Thus, although alcohol-associated sleep problems have significant economic and clinical consequences, very little is known about how and where alcohol acts to affect sleep. In this review, we have described our attempts to understand how and where alcohol acts to affect sleep. We have conducted a series of experiments using two different species, rats and mice, as animal models, and a combination of multi-disciplinary experimental methodologies to examine and understand anatomical and cellular substrates mediating the effects of acute and chronic alcohol exposure on sleep-wakefulness. The results of our studies suggest that the sleep-promoting effects of alcohol may be mediated via alcohol’s action on the mediators of sleep homeostasis: adenosine (AD) and the wake-promoting cholinergic neurons of the basal forebrain (BF). Alcohol, via its action on AD uptake, increases extracellular AD resulting in the inhibition of BF wake-promoting neurons. Lesions of the BF cholinergic neurons or blockade of AD A1 receptors results in attenuation of alcohol-induced sleep promotion, suggesting that AD and BF cholinergic neurons are critical for sleep-promoting effects of alcohol. Since binge alcohol consumption is a highly prevalent pattern of alcohol consumption and disrupts sleep, we examined the effects of binge drinking on sleep-wakefulness. Our results suggest that disrupted sleep homeostasis may be the primary cause of sleep disruption observed following binge drinking. Finally, we have also shown that insomnia and associated sleep disruptions, observed during acute withdrawal, are caused due to impaired sleep homeostasis. Based on our findings, we suggest that alcohol may disrupt sleep homeostasis to cause sleep disruptions.
DOI: 10.1016/s0006-8993(96)01263-2
发表时间: 1997-02-28
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