
수면 부족은 신피질의 AMPA 시냅스 강도와 수를 증가시키지만, 이는 수면 부족 반응의 일부분에 불과하다. 수면 부족은 2-3층 피라미드 뉴런의 AMPA/NMDA EPSC 비율을 증가시키고 침묵 시냅스를 감소시켜 LTP에 의한 활성화 시냅스로의 전환을 제한한다. 이러한 변화는 수면으로 회복된다.


coremsg

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

수면-요구에-의해-구동되는-글루타메르기성-시냅스-표현형의-진동


수면 요구에 의해 구동되는 글루타메르기성 시냅스 표현형의 진동
