Brain Plasticity and Local Sleep Homeostasis: An Electrophysiological

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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.