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: 7650158
• 负责人: GIULIO TONONI
• 金额: $ 18.49万
• 依托单位: UNIVERSITY OF WISCONSIN-MADISON
• 依托单位国家: 美国
• 资助国家: 美国
• 起止时间: 至
• 项目状态: 未结题
• 来源: https://reporter.nih.gov/project-details/7650158
• 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求的标志，随着 在睡眠期间，先前的清醒持续时间和指数降低。不幸的是，我们不知道 哪些生物过程是导致睡眠慢波增加随着觉醒的函数的原因，或 他们可以使用什么功能。根据最近的假设 - 突触稳态假设 睡眠功能 - 清醒期间发生的塑料过程导致突触强度的净增加 在许多皮质电路中。结果，当皮质神经元以低频开始振荡时 在睡眠期间，它们变得强烈同步，导致EEG慢幅度的慢速波。这些慢 波浪又负责突触强度的重新归一化，并对 能源代谢和性能。最近的工作表明，与假设一致 涉及特定皮质区域的视觉运动学习任务可导致慢波活动的局部增加 在随后的睡眠期间。这项工作还表明睡眠后的性能得到了提高，这 增强与慢波活性的局部增加相关。以这些结果为基础 项目将进一步测试两个突触稳态假设的至关重要的预测：睡眠慢波 i）学习后的皮质回路是必不可少的； ii）对于 睡眠后的性能增强。为此，使用轻度声学将抑制睡眠慢波 不会中断睡眠的刺激。因此，具体目的旨在评估是否按照 假设，学习留下了一个本地的脑电图痕迹，该轨迹在睡眠后重新归一致，以及选择性是否 剥夺睡眠慢波会导致这种脑电图的持续性。 性能提高。如果确认这些预测，它们将为 睡眠功能的突触稳态假设，并有助于解释项目I，III， 和IV。