Genes to Cognition Program, Centre for Clinical Brain Sciences, University of Edinburgh, Edinburgh EH16 4SB, UK.
Genes to Cognition Program, Centre for Clinical Brain Sciences, University of Edinburgh, Edinburgh EH16 4SB, UK; School of Science and Engineering, University of Dundee, Dundee DD1 4HN, UK.
Curr Biol. 2024 Aug 19;34(16):3836-3843.e5. doi: 10.1016/j.cub.2024.07.032. Epub 2024 Aug 2.
Insufficient sleep is a global problem with serious consequences for cognition and mental health. Synapses play a central role in many aspects of cognition, including the crucial function of memory consolidation during sleep. Interference with the normal expression or function of synapse proteins is a cause of cognitive, mood, and other behavioral problems in over 130 brain disorders. Sleep deprivation (SD) has also been reported to alter synapse protein composition and synapse number, although with conflicting results. In our study, we conducted synaptome mapping of excitatory synapses in 125 regions of the mouse brain and found that sleep deprivation selectively reduces synapse diversity in the cortex and in the CA1 region of the hippocampus. Sleep deprivation targeted specific types and subtypes of excitatory synapses while maintaining total synapse density (synapse number/area). Synapse subtypes with longer protein lifetimes exhibited resilience to sleep deprivation, similar to observations in aging and genetic perturbations. Moreover, the altered synaptome architecture affected the responses to neural oscillations, suggesting that sleep plays a vital role in preserving cognitive function by maintaining the brain's synaptome architecture.
睡眠不足是一个全球性问题，对认知和心理健康有严重影响。突触在认知的许多方面都起着核心作用，包括睡眠期间记忆巩固的关键功能。突触蛋白的正常表达或功能障碍是 130 多种脑部疾病引起认知、情绪和其他行为问题的原因。尽管结果存在冲突，但睡眠剥夺也被报道会改变突触蛋白的组成和突触数量。在我们的研究中，我们对小鼠大脑的 125 个区域进行了兴奋性突触的突触组图谱绘制，发现睡眠剥夺会选择性地减少皮质和海马 CA1 区的突触多样性。睡眠剥夺靶向特定类型和亚型的兴奋性突触，同时保持总突触密度（突触数量/面积）。具有较长蛋白寿命的突触亚型对睡眠剥夺具有更强的抵抗力，这与衰老和遗传干扰的观察结果相似。此外，改变的突触组图谱会影响对神经振荡的反应，这表明睡眠通过维持大脑的突触组图谱在维持认知功能方面起着至关重要的作用。
