<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><submitter>Madasu SC</submitter><funding>NIGMS NIH HHS</funding><pubmed_abstract>The voltage gated potassium channel Kv1.2 plays a key role in the central nervous system and mutations in Kv1.2 leads to neurological disorders such as epilepsies and ataxias. In the cerebellum regulation of Kv1.2 is coupled to learning and memory. We have previously shown that blocking Kv1.2 by infusing its specific inhibitor Tityustoxin-kα (TsTX) into the lobulus simplex of the cerebellum facilitates eyeblink conditioning (EBC) and that EBC modulates Kv1.2 surface expression in cerebellar interneurons. The metabotropic glutamate receptor mGluR1 is required for EBC although the molecular mechanisms are not fully understood. We have previously shown that infusion of the mGluR1 agonist (S)-3,5-dihydroxyphenylglycine (DHPG) into the lobulus simplex of the cerebellum mimics the faciliatory ef</pubmed_abstract><journal>bioRxiv : the preprint server for biology</journal><pagination>2025.11.09.687499</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12642406</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Anti-Kv1.2 Immunoprecipitation Identifies shared mGluR1-Associated Signalosome Complex proteins and PKC-Mediated Regulation of Kv1.2 in the Cerebellum.</pubmed_title><pmcid>PMC12642406</pmcid><funding_grant_id>P20 GM103449</funding_grant_id><pubmed_authors>Madasu SC</pubmed_authors><pubmed_authors>Morielli AD</pubmed_authors></additional><is_claimable>false</is_claimable><name>Anti-Kv1.2 Immunoprecipitation Identifies shared mGluR1-Associated Signalosome Complex proteins and PKC-Mediated Regulation of Kv1.2 in the Cerebellum.</name><description>The voltage gated potassium channel Kv1.2 plays a key role in the central nervous system and mutations in Kv1.2 leads to neurological disorders such as epilepsies and ataxias. In the cerebellum regulation of Kv1.2 is coupled to learning and memory. We have previously shown that blocking Kv1.2 by infusing its specific inhibitor Tityustoxin-kα (TsTX) into the lobulus simplex of the cerebellum facilitates eyeblink conditioning (EBC) and that EBC modulates Kv1.2 surface expression in cerebellar interneurons. The metabotropic glutamate receptor mGluR1 is required for EBC although the molecular mechanisms are not fully understood. We have previously shown that infusion of the mGluR1 agonist (S)-3,5-dihydroxyphenylglycine (DHPG) into the lobulus simplex of the cerebellum mimics the faciliatory ef</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Nov</publication><modification>2026-06-11T03:19:12.435Z</modification><creation>2026-06-11T03:08:24.758Z</creation></dates><accession>S-EPMC12642406</accession><cross_references><pubmed>41292836</pubmed><doi>10.1101/2025.11.09.687499</doi></cross_references></HashMap>