Menarchek Benjamin J, Bridi Michelle C D
Rockefeller Neuroscience Institute, West Virginia University, Morgantown, WV 26505, USA.
Rockefeller Neuroscience Institute, West Virginia University, Morgantown, WV 26505, USA.
Curr Opin Neurobiol. 2025 Aug;93:103029. doi: 10.1016/j.conb.2025.103029. Epub 2025 Apr 22.
Sleep is thought to serve an important role in learning and memory, but the mechanisms by which sleep promotes plasticity remain unclear. Even in the absence of plastic changes in neuronal function, many molecular, cellular, and physiological processes linked to plasticity are upregulated during sleep. Therefore, sleep may be a state in which latent plasticity mechanisms are poised to respond following novel experiences during prior wake. Many of these plasticity-related processes can promote both synaptic strengthening and weakening. Signaling pathways activated during sleep may interact with complements of proteins, determined by the content of prior waking experience, to establish the polarity of plasticity. Furthermore, precise reactivation of neuronal spiking patterns during sleep may interact with ongoing neuromodulatory, dendritic, and network activity to strengthen and weaken synapses. In this review, we will discuss the idea that sleep elevates latent plasticity mechanisms, which drive bidirectional plasticity depending on prior waking experience.
睡眠被认为在学习和记忆中发挥着重要作用,但睡眠促进可塑性的机制仍不清楚。即使在神经元功能没有可塑性变化的情况下,许多与可塑性相关的分子、细胞和生理过程在睡眠期间也会上调。因此,睡眠可能是一种状态,在这种状态下,潜在的可塑性机制准备好在先前清醒时的新体验后做出反应。许多这些与可塑性相关的过程既可以促进突触增强,也可以促进突触减弱。睡眠期间激活的信号通路可能与由先前清醒经历的内容决定的蛋白质互补物相互作用,以建立可塑性的极性。此外,睡眠期间神经元放电模式的精确重新激活可能与正在进行的神经调节、树突和网络活动相互作用,以增强和减弱突触。在这篇综述中,我们将讨论睡眠提升潜在可塑性机制的观点,这种机制根据先前的清醒经历驱动双向可塑性。