{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Vogt KE"],"funding":["AMEDD","NIDCD NIH HHS","NINDS NIH HHS","James S. McDonnell Foundation","NIDOCM"],"pagination":["RP98280"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11828481"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["13"],"pubmed_abstract":["Sleep loss increases AMPA-synaptic strength and number in the neocortex. However, this is only part of the synaptic sleep loss response. We report an 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. Sleep genes can thus provide a framework within which motor learn"],"journal":["eLife"],"pubmed_title":["Sleep need driven oscillation of glutamate synaptic phenotype."],"pmcid":["PMC11828481"],"funding_grant_id":["DC014702","10.37717/220020467","R01 DC014702","JP21zf0127005","R01 NS103422","NS103422"],"pubmed_authors":["Kulkarni A","Vogt KE","Konopka G","Pandey R","Dehnad M","Greene RW"],"additional_accession":[]},"is_claimable":false,"name":"Sleep need driven oscillation of glutamate synaptic phenotype.","description":"Sleep loss increases AMPA-synaptic strength and number in the neocortex. However, this is only part of the synaptic sleep loss response. We report an 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. Sleep genes can thus provide a framework within which motor learn","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Feb","modification":"2025-04-25T17:55:42.157Z","creation":"2025-04-25T17:55:42.157Z"},"accession":"S-EPMC11828481","cross_references":{"pubmed":["39950545"],"doi":["10.7554/eLife.98280"]}}