{"database":"biostudies-literature","file_versions":[],"scores":{"citationCount":0,"reanalysisCount":0,"viewCount":59,"searchCount":0},"additional":{"submitter":["Sheng N"],"funding":["HHS | NIH | National Institute of Mental Health","Ministry of Science and Technology of the People's Republic of China","the Chinese Academy of Sciences Pioneer Hundred Talents Program","NIMH NIH HHS","the Strategy Priority Research Program of the Chinese Academy of Sciences","National Natural Science Foundation of China","Natural Science Foundation of Jiangsu Province Grant"],"pagination":["3948-3953"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC5899490"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["115(15)"],"pubmed_abstract":["Long-term potentiation (LTP) is a persistent strengthening of synaptic transmission in the brain and is arguably the most compelling cellular and molecular model for learning and memory. Previous work found that both AMPA receptors and exogenously expressed kainate receptors are equally capable of expressing LTP, despite their limited homology and their association with distinct auxiliary subunits, indicating that LTP is far more promiscuous than previously thought. What might these two subtypes of glutamate receptor have in common? Using a single-cell molecular replacement strategy, we demonstrate that the AMPA receptor auxiliary subunit TARP γ-8, via its PDZ-binding motif, is indispensable for both basal synaptic transmission and LTP. Remarkably, kainate receptors and their auxiliary subunits Neto proteins share the same requirement of PDZ-binding domains for synaptic trafficking and LTP. Together, these results suggest that a minimal postsynaptic requirement for LTP is the PDZ binding of glutamate receptors/auxiliary subunits to PSD scaffolding proteins."],"journal":["Proceedings of the National Academy of Sciences of the United States of America"],"pubmed_title":["LTP requires postsynaptic PDZ-domain interactions with glutamate receptor/auxiliary protein complexes."],"pmcid":["PMC5899490"],"funding_grant_id":["N/A","R01 MH080379","R01MH070957","31741055","BK20140018","31571060","R56MH070957","XDB13000000","2014CB942804","31371061","R01MH080379","2015BAI08B02","R01 MH070957"],"pubmed_authors":["Nicoll RA","Tao W","Sheng N","Diaz-Alonso J","Shi YS","Bemben MA"],"view_count":["59"],"additional_accession":[]},"is_claimable":false,"name":"LTP requires postsynaptic PDZ-domain interactions with glutamate receptor/auxiliary protein complexes.","description":"Long-term potentiation (LTP) is a persistent strengthening of synaptic transmission in the brain and is arguably the most compelling cellular and molecular model for learning and memory. Previous work found that both AMPA receptors and exogenously expressed kainate receptors are equally capable of expressing LTP, despite their limited homology and their association with distinct auxiliary subunits, indicating that LTP is far more promiscuous than previously thought. What might these two subtypes of glutamate receptor have in common? Using a single-cell molecular replacement strategy, we demonstrate that the AMPA receptor auxiliary subunit TARP γ-8, via its PDZ-binding motif, is indispensable for both basal synaptic transmission and LTP. Remarkably, kainate receptors and their auxiliary subunits Neto proteins share the same requirement of PDZ-binding domains for synaptic trafficking and LTP. Together, these results suggest that a minimal postsynaptic requirement for LTP is the PDZ binding of glutamate receptors/auxiliary subunits to PSD scaffolding proteins.","dates":{"release":"2018-01-01T00:00:00Z","publication":"2018 Apr","modification":"2024-12-04T10:37:50.318Z","creation":"2019-03-26T23:59:40Z"},"accession":"S-EPMC5899490","cross_references":{"pubmed":["29581259"],"doi":["10.1073/pnas.1800719115"]}}