Sleep is a well conserved behaviour, 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. Many studies have found changes in neuronal architecture following sleep deprivation, but findings vary widely. This study provides the first systematic review of the effects of sleep deprivation on dendritic architecture.We searched MEDLINE and Web of Science for rodent studies which reported dendritic spine density and/or dendritic length after sleep deprivation 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 were high between studies, indicating substantial methodological differences. We therefore developed a protocol for quality assessment of sleep deprivation 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 h or less of sleep deprivation on dendritic structure. Chronic sleep deprivation protocols of 72 h or longer causes a decrease in 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.

Keywords: Sleep Deprivation; Synaptic plasticity dendritic plasticity; dendritic architecture; gentle handling.

© The Author(s) 2025. Published by Oxford University Press on behalf of Sleep Research Society.

睡眠是一种高度保守的行为，但其功能仍然不确定且存在争议。突触稳态假说提出睡眠在其中扮演着核心角色，并预测睡眠剥夺后全局突触强度会增加。许多研究发现睡眠剥夺后神经元结构发生变化，但是这些发现差异很大。本研究提供了对睡眠剥夺影响树突结构的首个系统性回顾。

我们检索了 MEDLINE 和 Web of Science 中的小鼠研究文献，筛选出报告了与对照组相比在睡眠剥夺后的树突棘密度和/或树突长度变化的文章。总共筛选了 5090 条记录，并选择其中30篇全文用于此次荟萃分析。这些研究样本量较小且数据处理方面的报道质量较差。不同研究之间的结构测量变量存在较大差异，这表明方法学上有显著区别。因此我们制定了一个评估睡眠剥夺和树突/棘结构分析的质量协议，可作为未来研究的框架。我们也基于所包含的研究模拟了实验并展示了小样本量会导致效应大小估计过高。结论是现有证据不支持24小时或更短时间内的睡眠剥夺对树突结构产生影响。然而72小时以上的慢性睡眠剥夺会减少CA1区域（海马体的一部分）的树突棘密度和树突长度，但尚不清楚这是由于睡眠不足还是实验诱发的压力所致。

本研究提供了对该领域内存在矛盾发现的一个有价值的概述，并阐明了哪些问题阻碍了得出坚实结论。在这个领域的进一步进展需要更好地处理多层次数据、更清晰地指导树突结构测量以及更大样本量的研究。

关键词：睡眠剥夺；突触可塑性，树突发育可塑性；树突结构；轻柔处理。

© The Author(s) 2025. Published by Oxford University Press on behalf of Sleep Research Society.