<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Sharma B</submitter><funding>NIA NIH HHS</funding><funding>NINDS NIH HHS</funding><pagination>2698-2707</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11168514</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>19(12)</volume><pubmed_abstract>JOURNAL/nrgr/04.03/01300535-202412000-00026/figure1/v/2024-04-08T165401Z/r/image-tiff Gamma-aminobutyric acid (GABA)ergic neurons, the most abundant inhibitory neurons in the human brain, have been found to be reduced in many neurological disorders, including Alzheimer's disease and Alzheimer's disease-related dementia. Our previous study identified the upregulation of microRNA-502-3p (miR-502-3p) and downregulation of GABA type A receptor subunit α-1 in Alzheimer's disease synapses. This study investigated a new molecular relationship between miR-502-3p and GABAergic synapse function. In vitro studies were performed using the mouse hippocampal neuronal cell line HT22 and miR-502-3p agomiRs and antagomiRs. In silico analysis identified multiple binding sites of miR-502-3p at GABA type A re</pubmed_abstract><journal>Neural regeneration research</journal><pubmed_title>MicroRNA-502-3p regulates GABAergic synapse function in hippocampal neurons.</pubmed_title><pmcid>PMC11168514</pmcid><funding_grant_id>R00 AG065645</funding_grant_id><funding_grant_id>K99 AG065645</funding_grant_id><funding_grant_id>R01 NS115834</funding_grant_id><pubmed_authors>Sharma B</pubmed_authors><pubmed_authors>Rodriguez S</pubmed_authors><pubmed_authors>Torres MM</pubmed_authors><pubmed_authors>Gangwani L</pubmed_authors><pubmed_authors>Kumar S</pubmed_authors></additional><is_claimable>false</is_claimable><name>MicroRNA-502-3p regulates GABAergic synapse function in hippocampal neurons.</name><description>JOURNAL/nrgr/04.03/01300535-202412000-00026/figure1/v/2024-04-08T165401Z/r/image-tiff Gamma-aminobutyric acid (GABA)ergic neurons, the most abundant inhibitory neurons in the human brain, have been found to be reduced in many neurological disorders, including Alzheimer's disease and Alzheimer's disease-related dementia. Our previous study identified the upregulation of microRNA-502-3p (miR-502-3p) and downregulation of GABA type A receptor subunit α-1 in Alzheimer's disease synapses. This study investigated a new molecular relationship between miR-502-3p and GABAergic synapse function. In vitro studies were performed using the mouse hippocampal neuronal cell line HT22 and miR-502-3p agomiRs and antagomiRs. In silico analysis identified multiple binding sites of miR-502-3p at GABA type A re</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Dec</publication><modification>2026-07-04T03:14:04.703Z</modification><creation>2026-07-04T03:11:00.697Z</creation></dates><accession>S-EPMC11168514</accession><cross_references><pubmed>38595288</pubmed><doi>10.4103/NRR.NRR-D-23-01064</doi></cross_references></HashMap>