Child Development Center, University Children's Hospital Zürich, Zürich, Switzerland.
Prog Brain Res. 2011;193:63-82. doi: 10.1016/B978-0-444-53839-0.00005-3.
Sleep slow waves are the major electrophysiological features of non-rapid eye movement (NREM) sleep. Although there is growing understanding of where slow waves originate and how they are generated during sleep, the function of slow waves is still largely unclear. A recently proposed hypothesis relates slow waves to the homeostatic regulation of synaptic plasticity. While several studies confirm a correlation between experimentally triggered synaptic changes and slow-wave activity (SWA), little is known about its association to synaptic changes occurring during cortical maturation. Interestingly, slow waves undergo remarkable changes during development that parallel the time course of cortical maturation. In a recent cross-sectional study including children and adolescents, the topographical distribution of SWA was analyzed with high-density electroencephalography. The results showed age-dependent differences in SWA topography: SWA was highest over posterior regions during early childhood and then shifted over central derivations to the frontal cortex in late adolescence. This trajectory of SWA topography matches the course of cortical gray maturation. In this chapter, the major changes in slow waves during development are highlighted and linked to cortical maturation and behavior. Interestingly, synaptic density and slow-wave amplitude increase during childhood are highest shortly before puberty, decline thereafter during adolescence, reaching overall stable levels during adulthood. The question arises whether SWA is merely reflecting cortical changes or if it plays an active role in brain maturation. We thereby propose a model, by which sleep slow waves may contribute to cortical maturation. We hypothesize that while there is a balance between synaptic strengthening and synaptic downscaling in adults, the balance of strengthening/formation and weakening/elimination is tilted during development.
睡眠慢波是非快速眼动（NREM）睡眠的主要电生理特征。尽管人们越来越了解慢波的起源以及它们在睡眠中是如何产生的，但慢波的功能仍然很大程度上不清楚。最近提出的一个假设将慢波与突触可塑性的稳态调节联系起来。虽然几项研究证实了实验触发的突触变化与慢波活动（SWA）之间存在相关性，但对于皮质成熟过程中发生的突触变化与 SWA 的相关性知之甚少。有趣的是，慢波在发育过程中发生了显著的变化，与皮质成熟的时间进程平行。在最近的一项包括儿童和青少年的横断面研究中，使用高密度脑电图分析了 SWA 的拓扑分布。结果表明 SWA 拓扑存在年龄依赖性差异：在幼儿期，SWA 在后头部区域最高，然后在前额皮质的中央部位转移。这种 SWA 拓扑的轨迹与皮质灰质成熟的过程相匹配。在这一章中，强调了发育过程中慢波的主要变化，并将其与皮质成熟和行为联系起来。有趣的是，儿童期的突触密度和慢波幅度增加在青春期前最高，此后在青春期下降，在成年期达到总体稳定水平。问题是 SWA 是否仅仅反映了皮质变化，还是它在大脑成熟中发挥了积极作用。因此，我们提出了一个模型，通过该模型，睡眠慢波可能有助于皮质成熟。我们假设，虽然在成年人中存在突触增强和突触缩小之间的平衡，但在发育过程中，增强/形成和削弱/消除之间的平衡是倾斜的。
