Sleep deprivation and dendritic architecture: a systematic review and meta-analysis.

IF 4.9 2区 医学 Q1 Medicine
Sleep Pub Date : 2025-09-09 DOI:10.1093/sleep/zsaf146
Alvin T S Brodin, Franziska Liesecke, Julia Spielbauer, Tobias E Karlsson
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Abstract

Sleep is a well-conserved behavior, yet the functions of sleep remain uncertain and controversial. The synaptic homeostasis hypothesis proposes a central role for sleep, predicting that global synaptic strength increases after sleep deprivation (SD). Many studies have found changes in neuronal architecture following SD, but findings vary widely. This study provides the first systematic review of the effects of SD on dendritic architecture. We searched MEDLINE and Web of Science for rodent studies which reported dendritic spine density and/or dendritic length after SD compared to control. A total of 5090 records were screened, yielding 30 full texts for this meta-analysis. Studies were individually small and suffered from poor reporting regarding handling of data. Variability in structural measures was high between studies, indicating substantial methodological differences. We therefore developed a protocol for quality assessment of SD and spine/dendrite analysis, which can serve as framework for future studies. We also simulated experiments based on the included studies and showed that small sample sizes result in an overestimation of effect sizes. We conclude that current evidence does not support an effect from 24 hours or less of SD on dendritic structure. Chronic SD protocols of 72 hours or longer causes a decrease in Cornu Ammonis 1 (CA1), both in spine density and dendritic length, but it remains unclear whether this is a result of sleep loss or protocol-induced stress. This study provides a valuable overview of a field marked by conflicting findings, and clarifies which issues prevent robust conclusions from being drawn. Further progress in this field requires more robust handling of multi-level data, clearer guidelines on dendritic structure measurements and substantially higher-powered studies.

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睡眠剥夺和树突结构:系统回顾和荟萃分析。
睡眠是一种保守的行为,但睡眠的功能仍然不确定和有争议。突触内稳态假说提出了睡眠的核心作用,预测睡眠剥夺后整体突触强度会增加。许多研究都发现了睡眠剥夺后神经元结构的变化,但研究结果差异很大。这项研究首次系统地回顾了睡眠剥夺对树突结构的影响。我们在MEDLINE和Web of Science上搜索了啮齿动物的研究,这些研究报告了睡眠剥夺后与对照组相比的树突脊柱密度和/或树突长度。总共筛选了5090份记录,为本荟萃分析提供了30份全文。个别研究规模较小,并且在数据处理方面报告不足。研究之间结构测量的可变性很高,表明方法上存在实质性差异。因此,我们制定了睡眠剥夺质量评估和脊柱/树突分析的协议,可以作为未来研究的框架。我们还在纳入的研究基础上进行了模拟实验,结果表明,小样本量会导致对效应量的高估。我们的结论是,目前的证据不支持24小时或更少的睡眠剥夺对树突结构的影响。72小时或更长时间的慢性睡眠剥夺方案导致CA1降低,脊柱密度和树突长度均下降,但尚不清楚这是睡眠不足还是方案引起的压力的结果。这项研究提供了一个有价值的概述,以相互矛盾的发现为标志的领域,并澄清了哪些问题阻碍了得出强有力的结论。这一领域的进一步进展需要更强大的多层次数据处理,更清晰的树突结构测量指南和更有力的研究。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Sleep
Sleep Medicine-Neurology (clinical)
CiteScore
8.70
自引率
10.70%
发文量
0
期刊介绍: SLEEP® publishes findings from studies conducted at any level of analysis, including: Genes Molecules Cells Physiology Neural systems and circuits Behavior and cognition Self-report SLEEP® publishes articles that use a wide variety of scientific approaches and address a broad range of topics. These may include, but are not limited to: Basic and neuroscience studies of sleep and circadian mechanisms In vitro and animal models of sleep, circadian rhythms, and human disorders Pre-clinical human investigations, including the measurement and manipulation of sleep and circadian rhythms Studies in clinical or population samples. These may address factors influencing sleep and circadian rhythms (e.g., development and aging, and social and environmental influences) and relationships between sleep, circadian rhythms, health, and disease Clinical trials, epidemiology studies, implementation, and dissemination research.
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