{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Tseng WC"],"funding":["Howard Hughes Medical Institute","George Barth Geller fund","NIDCD NIH HHS"],"pagination":["1214-9"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4313813"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["112(4)"],"pubmed_abstract":["GABAA-receptor-based interneuron circuitry is essential for higher order function of the human nervous system and is implicated in schizophrenia, depression, anxiety disorders, and autism. Here we demonstrate that giant ankyrin-G (480-kDa ankyrin-G) promotes stability of somatodendritic GABAergic synapses in vitro and in vivo. Moreover, giant ankyrin-G forms developmentally regulated and cell-type-specific micron-scale domains within extrasynaptic somatodendritic plasma membranes of pyramidal neurons. We further find that giant ankyrin-G promotes GABAergic synapse stability through opposing endocytosis of GABAA receptors, and requires a newly described interaction with GABARAP, a GABAA receptor-associated protein. We thus present a new mechanism for stabilization of GABAergic interneuron s"],"journal":["Proceedings of the National Academy of Sciences of the United States of America"],"pubmed_title":["Giant ankyrin-G stabilizes somatodendritic GABAergic synapses through opposing endocytosis of GABAA receptors."],"pmcid":["PMC4313813"],"funding_grant_id":["N/A","R01 DC002524"],"pubmed_authors":["Jenkins PM","Mooney R","Tseng WC","Bennett V","Tanaka M"],"additional_accession":[]},"is_claimable":false,"name":"Giant ankyrin-G stabilizes somatodendritic GABAergic synapses through opposing endocytosis of GABAA receptors.","description":"GABAA-receptor-based interneuron circuitry is essential for higher order function of the human nervous system and is implicated in schizophrenia, depression, anxiety disorders, and autism. Here we demonstrate that giant ankyrin-G (480-kDa ankyrin-G) promotes stability of somatodendritic GABAergic synapses in vitro and in vivo. Moreover, giant ankyrin-G forms developmentally regulated and cell-type-specific micron-scale domains within extrasynaptic somatodendritic plasma membranes of pyramidal neurons. We further find that giant ankyrin-G promotes GABAergic synapse stability through opposing endocytosis of GABAA receptors, and requires a newly described interaction with GABARAP, a GABAA receptor-associated protein. We thus present a new mechanism for stabilization of GABAergic interneuron s","dates":{"release":"2015-01-01T00:00:00Z","publication":"2015 Jan","modification":"2025-04-21T19:48:44.975Z","creation":"2019-03-27T01:44:25Z"},"accession":"S-EPMC4313813","cross_references":{"pubmed":["25552561"],"doi":["10.1073/pnas.1417989112"]}}