Brain Plasticity and Local Sleep Homeostasis: An Electrophysiological

大脑可塑性和局部睡眠稳态：电生理学

• 批准号: 7346831
• 负责人: GIULIO TONONI
• 金额: $ 21.06万
• 依托单位: UNIVERSITY OF WISCONSIN-MADISON
• 依托单位国家: 美国
• 财政年份: 2007
• 资助国家: 美国
• 起止时间: 2007-09-27 至 2011-06-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7346831
• 关键词: Acoustic Stimulation; Acoustics; Area; Biological Process; Brain; Cerebral cortex; Computers; Disease; Electroencephalogram; Electroencephalography; Energy Metabolism; Event; Figs - dietary; Frequencies; Health; Homeostasis; Human; Learning; Left; Location; Magnetic Resonance Imaging; Mammals; Mental disorders; Metabolic; Middle Insomnia; Neurologic; Neurons; Parietal Lobe; Performance; Plastics; Play; Process; Regulation; Role; Rotation; Signal Transduction; Sleep; Sleep Deprivation; Slow-Wave Sleep; Stage II Sleep; Stimulus; Synapses; Synaptic plasticity; Testing; Therapeutic; Wakefulness; Work; base; computerized; design; human subject; kinematics; motor control; neural circuit; novel; pressure; prevent; research study; sleep regulation; visual motor

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.

睡眠脑电图（EEC）中的慢波活动是睡眠需要的标志，随着睡眠时间的增加而增加。 先前清醒的持续时间并在睡眠期间呈指数级下降。不幸的是，我们不知道 哪种生物过程负责作为觉醒的函数的睡眠慢波的增加，或者 它们可以发挥什么作用。根据最近的一个假说-突触稳态假说， 睡眠功能--在清醒时发生的可塑性过程导致突触强度的净增加 在许多皮层回路中。因此，当皮层神经元开始以低频率振荡时， 在睡眠期间，它们变得强烈同步，导致高振幅的EEG慢波。这些缓慢 波，反过来，负责突触强度的重新正常化， 能量代谢和性能。最近的研究表明，与假设一致， 涉及特定皮层区域的视觉学习任务导致慢波活动的局部增加 在随后的睡眠中。这项研究还表明，睡眠后的表现会增强， 增强与慢波活动的局部增加相关。基于这些结果，这 该项目将进一步测试突触稳态假说的两个关键预测：睡眠慢波 i）是学习后皮质回路重新正常化所必需的; ii）是学习后皮质回路重新正常化所必需的。 增强睡眠后的表现。要做到这一点，睡眠慢波将被抑制使用温和的声学 不影响睡眠的刺激。因此，具体目标的设计是为了评估， 假设，学习会留下一个局部的脑电图轨迹，在睡眠后重新正常化，以及选择性的 剥夺睡眠慢波会导致这种EEG痕迹的持续存在，并抑制睡眠后的 性能增强。如果这些预测得到证实， 睡眠功能的突触稳态假说，并有助于解释项目I，III， 和IV.