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Net decrease in spine-surface GluA1-containing AMPA receptors after post-learning sleep in the adult mouse cortex
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DOI：10.1038/s41467-021-23156-2.png)
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Abstract
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The mechanisms by which sleep benefits learning and memory remain unclear. Sleep may further strengthen the synapses potentiated by learning or promote broad synaptic weakening while protecting the newly potentiated synapses. We tested these ideas by combining a motor task whose consolidation is sleep-dependent, a marker of synaptic AMPA receptor plasticity, and repeated two-photon imaging to track hundreds of spines in vivo with single spine resolution. In mouse motor cortex, sleep leads to an overall net decrease in spine-surface GluA1-containing AMPA receptors, both before and after learning. Molecular changes in single spines during post-learning sleep are correlated with changes in performance after sleep. The spines in which learning leads to the largest increase in GluA1 expression have a relative advantage after post-learning sleep compared to sleep deprivation, because sleep weakens all remaining spines. These results are obtained in adult mice, showing that sleep-dependent synaptic down-selection also benefits the mature brain. The synaptic mechanisms of how sleep benefits cognitive functions are not well characterised. Here, the authors show that sleep leads to an overall net decrease in spine-surface GluA1-containing AMPA receptors and that this is correlated with changes in performance after sleep.
Keywords:
LONG-TERM POTENTIATION
SYNAPTIC PLASTICITY
NEUROCOGNITIVE CONSEQUENCES
MEMORY CONSOLIDATION
WAKE
TRAFFICKING
HOMEOSTASIS
EXPRESSION
DEPRESSION
SYNAPSES
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