Seibt Julie, Frank Marcos G
Surrey Sleep Research Centre, University of Surrey, Guildford, United Kingdom.
Department of Biomedical Sciences, Elson S. Floyd College of Medicine, Washington State University Spokane, Spokane, WA, United States.
Front Syst Neurosci. 2019 Feb 1;13:2. doi: 10.3389/fnsys.2019.00002. eCollection 2019.
It is commonly accepted that brain plasticity occurs in wakefulness sleep. However, how these different brain states work in concert to create long-lasting changes in brain circuitry is unclear. Considering that wakefulness and sleep are profoundly different brain states on multiple levels (e.g., cellular, molecular and network activation), it is unlikely that they operate exactly the same way. Rather it is probable that they engage different, but coordinated, mechanisms. In this article we discuss how plasticity may be divided across the sleep-wake cycle, and how synaptic changes in each brain state are linked. Our working model proposes that waking experience triggers short-lived synaptic events that are necessary for transient plastic changes and mark (i.e., 'prime') circuits and synapses for further processing in sleep. During sleep, synaptic protein synthesis at primed synapses leads to structural changes necessary for long-term information storage.
人们普遍认为大脑可塑性发生在清醒和睡眠状态中。然而,尚不清楚这些不同的脑状态如何协同作用以在脑回路中产生持久变化。鉴于清醒和睡眠在多个层面(例如细胞、分子和网络激活)上是截然不同的脑状态,它们不太可能以完全相同的方式运作。相反,它们可能采用不同但相互协调的机制。在本文中,我们讨论了可塑性如何在睡眠-清醒周期中划分,以及每种脑状态下的突触变化是如何联系的。我们的工作模型提出,清醒经历会触发短暂的突触事件,这些事件对于瞬时可塑性变化是必要的,并标记(即“启动”)回路和突触以便在睡眠中进行进一步处理。在睡眠期间,启动突触处的突触蛋白合成会导致长期信息存储所需的结构变化。