Brain Plasticity and Local Sleep Homeostasis: An Electrophysiological

睡眠脑电(EEC)中的慢波活动是睡眠需要的标志，随着年龄的增加，慢波活动增加 先前清醒的持续时间，并在睡眠期间呈指数递减。不幸的是，我们不知道 下列哪种生物过程导致睡眠慢波作为清醒状态的函数而增加，或者 它们可能起到什么作用。根据最近的一项假说--突触动态平衡假说 睡眠功能--清醒时发生的可塑性过程会导致突触强度的净增加 在许多大脑皮层回路中。因此，当皮质神经元开始以低频振荡时 在睡眠期间，它们变得强烈同步，导致脑电慢波的高幅度。这些都很慢 反过来，波负责突触强度的重整化，并对 能量代谢和表现。最近的研究表明，与假设一致，一个 涉及特定皮质区域的视觉运动学习任务会导致局部慢波活动增加 在随后的睡眠中。这项研究还表明，睡眠后的表现会增强，这一点 增强与局部慢波活动增加相关。在这些结果的基础上，这 该项目将进一步检验突触动态平衡假说的两个关键预测：睡眠慢波 I)是学习后大脑皮层环路重整化所必需的；以及ii)是 睡眠后表现的增强。要做到这一点，睡眠慢波将被用温和的声学方法抑制 不会打断睡眠的刺激。因此，具体目标旨在评估是否如所预测的那样 假设，学习会在睡眠后留下局部脑电痕迹，而选择性脑电 剥夺睡眠慢波会导致这种脑电痕迹的持续，并导致睡眠后抑制 性能增强。如果这些预测得到证实，它们将为 睡眠功能的突触稳态假说和帮助解释项目I，III， 和IV。

Slow wave activity in the sleep electroencephalogram (EEC) is a marker of sleep need, increasing with the duration of prior wakefulness and decreasing exponentially during sleep. Unfortunately, we do not know which biological process is responsible for the increase of sleep slow waves as a function of wakefulness, or what function they may serve. According to a recent hypothesis - the synaptic homeostasis hypothesis of sleep function - plastic processes occurring during wakefulness result in a net increase in synaptic strength in many cortical circuits. As a consequence, when cortical neurons begin oscillating at low frequencies during sleep, they become strongly synchronized, leading to EEG slow waves of high amplitude. These slow waves, in turn, are responsible for the renormalization of synaptic strength and have beneficial effects on energy metabolism and performance. Recent work has shown that, consistent with the hypothesis, a visuomotor learning task that involves a specific cortical area leads to a local increase in slow wave activity during subsequent sleep. This work has also shown that performance is enhanced after sleep, and this enhancement is correlated with the local increase in slow wave activity. Building upon these results, this project will test two further, crucial predictions of the synaptic homeostasis hypothesis: that sleep slow waves i) are necessary for the renormalization of cortical circuits after learning; and ii) are necessary for the enhancement of performance after sleep. TO do so, sleep slow waves will be suppressed using mild acoustic stimuli that do not interrupt sleep. The specific aims are thus designed to evaluate whether, as predicted by the hypothesis, learning leaves a local EEG trace that is renormalized after sleep, and whether the selective deprivation of sleep slow waves leads to a persistence of such EEG traces.and to a suppression of postsleep performance enhancement. If these predictions are confirmed, they will lend strong support to the synaptic homeostasis hypothesis of sleep function and aid in the interpretation of the results of Projects I, III, and IV.