
睡眠欠乏は前頭皮質のピラミッド細胞のグルタミン酸作動性シナプスの AMPA/NMDA 比を増加させ、沈黙性シナプスを減少させる。これらの変化は睡眠によって回復する。これらの変化は、MEF2c およびHDAC4 転写因子によって制御される睡眠関連遺伝子群の発現変動によって仲介されている。


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Sleep loss increases AMPA-synaptic strength and number in the neocortex. However, this is only part of the synaptic sleep loss response. We report increased AMPA/NMDA EPSC ratio in frontal-cortical pyramidal neurons of layers 2-3. Silent synapses are absent, decreasing the plastic potential to convert silent NMDA to active AMPA synapses. These sleep loss changes are recovered by sleep. Sleep genes are enriched for synaptic shaping cellular components controlling glutamate synapse phenotype, overlap with autism risk genes and are primarily observed in excitatory pyramidal neurons projecting intra-telencephalically. These genes are enriched with genes controlled by the transcription factor, MEF2c and its repressor, HDAC4. Thus, sleep genes under the influence of MEF2c and HDAC4, can provide a framework within which motor learning and training occurs mediated by sleep-dependent oscillation of glutamate-synaptic phenotypes.

### Competing Interest Statement

The authors have declared no competing interest.

Sleep need driven oscillation of glutamate synaptic phenotype

睡眠需要に駆動されるグルタミン酸作動性シナプスの表現型の変動