<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>9(1)</volume><submitter>Lozovaya N</submitter><pubmed_abstract>We report that half striatal cholinergic interneurons are dual transmitter cholinergic and GABAergic interneurons (CGINs) expressing ChAT, GAD65, Lhx7, and Lhx6 mRNAs, labeled with GAD and VGAT, generating monosynaptic dual cholinergic/GABAergic currents and an inhibitory pause response. Dopamine deprivation increases CGINs ongoing activity and abolishes GABAergic inhibition including the cortico-striatal pause because of high [Cl-]i levels. Dopamine deprivation also dramatically increases CGINs dendritic arbors and monosynaptic interconnections probability, suggesting the formation of a dense CGINs network. The NKCC1 chloride importer antagonist bumetanide, which reduces [Cl-]i levels, restores GABAergic inhibition, the cortico-striatal pause-rebound response, and attenuates motor effects</pubmed_abstract><journal>Nature communications</journal><pagination>1422</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC5897332</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>GABAergic inhibition in dual-transmission cholinergic and GABAergic striatal interneurons is abolished in Parkinson disease.</pubmed_title><pmcid>PMC5897332</pmcid><pubmed_authors>Cloarec R</pubmed_authors><pubmed_authors>Riffault B</pubmed_authors><pubmed_authors>Dufour A</pubmed_authors><pubmed_authors>Burnashev N</pubmed_authors><pubmed_authors>Eftekhari S</pubmed_authors><pubmed_authors>Pons-Bennaceur A</pubmed_authors><pubmed_authors>Ben-Ari Y</pubmed_authors><pubmed_authors>Oumar N</pubmed_authors><pubmed_authors>Hammond C</pubmed_authors><pubmed_authors>Billon-Grand M</pubmed_authors><pubmed_authors>Gouty-Colomer LA</pubmed_authors><pubmed_authors>Lozovaya N</pubmed_authors></additional><is_claimable>false</is_claimable><name>GABAergic inhibition in dual-transmission cholinergic and GABAergic striatal interneurons is abolished in Parkinson disease.</name><description>We report that half striatal cholinergic interneurons are dual transmitter cholinergic and GABAergic interneurons (CGINs) expressing ChAT, GAD65, Lhx7, and Lhx6 mRNAs, labeled with GAD and VGAT, generating monosynaptic dual cholinergic/GABAergic currents and an inhibitory pause response. Dopamine deprivation increases CGINs ongoing activity and abolishes GABAergic inhibition including the cortico-striatal pause because of high [Cl-]i levels. Dopamine deprivation also dramatically increases CGINs dendritic arbors and monosynaptic interconnections probability, suggesting the formation of a dense CGINs network. The NKCC1 chloride importer antagonist bumetanide, which reduces [Cl-]i levels, restores GABAergic inhibition, the cortico-striatal pause-rebound response, and attenuates motor effects</description><dates><release>2018-01-01T00:00:00Z</release><publication>2018 Apr</publication><modification>2025-04-18T18:22:06.591Z</modification><creation>2019-03-26T23:29:35Z</creation></dates><accession>S-EPMC5897332</accession><cross_references><pubmed>29651049</pubmed><doi>10.1038/s41467-018-03802-y</doi></cross_references></HashMap>