{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Welle TM"],"funding":["HHS | NIH | National Institute of Mental Health","NIDA NIH HHS","HHS | NIH | National Institute of Neurological Disorders and Stroke (NINDS)","HHS | NIH | National Institute on Drug Abuse (NIDA)","HHS | NIH | National Institute of Neurological Disorders and Stroke","NIMH NIH HHS","HHS | NIH | National Institute on Drug Abuse","NINDS NIH HHS","HHS | NIH | National Institute of Mental Health (NIMH)"],"pagination":["5141-5168"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11549329"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["25(11)"],"pubmed_abstract":["Activity-dependent protein synthesis is crucial for long-lasting forms of synaptic plasticity. However, our understanding of translational mechanisms controlling GABAergic synapses is limited. One distinct form of inhibitory long-term potentiation (iLTP) enhances postsynaptic clusters of GABA<sub>A</sub>Rs and the primary inhibitory scaffold, gephyrin, to promote sustained synaptic strengthening. While we previously found that persistent iLTP requires mRNA translation, the mechanisms controlling plasticity-induced gephyrin translation remain unknown. We identify miR153 as a novel regulator of Gphn mRNA translation which controls gephyrin protein levels and synaptic clustering, ultimately impacting inhibitory synaptic structure and function. iLTP induction downregulates miR153, reversing it"],"journal":["EMBO reports"],"pubmed_title":["miRNA-mediated control of gephyrin synthesis drives sustained inhibitory synaptic plasticity."],"pmcid":["PMC11549329"],"funding_grant_id":["F30 DA048543","R01MH119154","FNS120640A","F30DA048543","R35NS116879","T32NS099042","R01DA35821","F31NS12410","F31 NS130979","R01 NS095809","F31NS130979","R01NS95809","R01 DA035821","R01 MH119154","R35 NS116879","T32 NS099042","R01 MH128199","R01 MH123700","R01MH128199","F99 NS120640"],"pubmed_authors":["Garcia JD","Ford CP","Kareemo DJ","Dell'Acqua ML","Welle TM","Martinez TP","Zych SM","Gookin SE","Kennedy MJ","Smith KR","Rajgor D","Wolfe SE"],"additional_accession":[]},"is_claimable":false,"name":"miRNA-mediated control of gephyrin synthesis drives sustained inhibitory synaptic plasticity.","description":"Activity-dependent protein synthesis is crucial for long-lasting forms of synaptic plasticity. However, our understanding of translational mechanisms controlling GABAergic synapses is limited. One distinct form of inhibitory long-term potentiation (iLTP) enhances postsynaptic clusters of GABA<sub>A</sub>Rs and the primary inhibitory scaffold, gephyrin, to promote sustained synaptic strengthening. While we previously found that persistent iLTP requires mRNA translation, the mechanisms controlling plasticity-induced gephyrin translation remain unknown. We identify miR153 as a novel regulator of Gphn mRNA translation which controls gephyrin protein levels and synaptic clustering, ultimately impacting inhibitory synaptic structure and function. iLTP induction downregulates miR153, reversing it","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Nov","modification":"2026-06-01T16:22:37.109Z","creation":"2025-04-04T11:42:15.524Z"},"accession":"S-EPMC11549329","cross_references":{"pubmed":["39294503"],"doi":["10.1038/s44319-024-00253-z"]}}