{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Liu Y"],"funding":["National Major Science and Technology Projects of China","Postdoctoral Research Foundation of China","National Natural Science Foundation of China and the Swedish Foundation for International Cooperation in Research and Education","National Natural Science Foundation of China"],"pagination":["1076"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12877408"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["9"],"pubmed_abstract":["While sleep disorders are a known correlate of social memory deficits, the underlying neurocircuitry and molecular mechanisms remain poorly understood. Using an oxytocin (OXT)-specific sensor imaging approach, we discovered that chronic sleep deprivation (SD) reduced OXT neuropeptide release in the hippocampal CA2 and prelimbic cortex (PrL), thereby disrupting social memory encoding and retrieval processes, respectively. Using fiber photometry recordings and in vitro electrophysiology, we identified the activity of the predominantly OXT-expressing neurons in the paraventricular hypothalamic nucleus (PVN<sup>OXT</sup>) were reduced following SD. Specific optogenetic activation of the PVN<sup>OXT</sup>-CA2 pathway during encoding phase or PVN<sup>OXT</sup>-PrL pathway during retrieval transi"],"journal":["Research (Washington, D.C.)"],"pubmed_title":["Decreased Oxytocin Mediates PVN-CA2 and PVN-PrL in Sleep Deprivation-Induced Social Memory Deficits."],"pmcid":["PMC12877408"],"funding_grant_id":["8201101416","2024M762504","32071140","82271960","SBGJ202501008","82472046"],"pubmed_authors":["Liu Y","Yi K","Li H","Rao B","Zhang Y","Gao Y","Wang Y","Bi L","Xu H","Deng Y","Cang Y"],"additional_accession":[]},"is_claimable":false,"name":"Decreased Oxytocin Mediates PVN-CA2 and PVN-PrL in Sleep Deprivation-Induced Social Memory Deficits.","description":"While sleep disorders are a known correlate of social memory deficits, the underlying neurocircuitry and molecular mechanisms remain poorly understood. Using an oxytocin (OXT)-specific sensor imaging approach, we discovered that chronic sleep deprivation (SD) reduced OXT neuropeptide release in the hippocampal CA2 and prelimbic cortex (PrL), thereby disrupting social memory encoding and retrieval processes, respectively. Using fiber photometry recordings and in vitro electrophysiology, we identified the activity of the predominantly OXT-expressing neurons in the paraventricular hypothalamic nucleus (PVN<sup>OXT</sup>) were reduced following SD. Specific optogenetic activation of the PVN<sup>OXT</sup>-CA2 pathway during encoding phase or PVN<sup>OXT</sup>-PrL pathway during retrieval transi","dates":{"release":"2026-01-01T00:00:00Z","publication":"2026","modification":"2026-07-10T03:24:06.268Z","creation":"2026-07-10T03:15:58.025Z"},"accession":"S-EPMC12877408","cross_references":{"pubmed":["41660638"],"doi":["10.34133/research.1076"]}}