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dc.contributor.authorAn, JJ-
dc.contributor.authorBae, MH-
dc.contributor.authorCho, SR-
dc.contributor.authorLee, SH-
dc.contributor.authorChoi, SH-
dc.contributor.authorLee, BH-
dc.contributor.authorShin, HS-
dc.contributor.authorKim, YN-
dc.contributor.authorPark, KW-
dc.contributor.authorBorrelli, E-
dc.contributor.authorBaik, JH-
dc.date.accessioned2024-01-21T07:14:06Z-
dc.date.available2024-01-21T07:14:06Z-
dc.date.created2021-09-02-
dc.date.issued2004-04-
dc.identifier.issn1044-7431-
dc.identifier.urihttps://pubs.kist.re.kr/handle/201004/137738-
dc.description.abstractThe levels of glutamic acid decarboxylase (GAD) were strongly increased in the cortex and the striatum in dopamine D2 receptors null (D2R-/-) mice, which show a significant locomotor impairment. In this study, the effects of different GABAergic drugs on locomotor,activity were analyzed in D2R-/- mice. After administering muscimol (1 mg/kg), a GABA(A) receptor agonist, the D2R-/- mice showed increased locomotor activity up to 200%. When the muscimol dose was increased (4-6 mg/kg), the D2R-/- mice exhibited seizure-like behavior, and the electroencephalographic (EEG) recordings during these behaviors showed a high amplitude rhythmic epileptiform activity in these mice. In situ hybridization showed that after injecting muscimol in the D2R-/- mice, the expression of enkephalin and immediate early gene, NGFI-A, was closely regulated with the locomotor activity regulated by GABAergic stimulation. These results suggest that the absence of D2R alters the GABAergic neurotransmission, specifically on GABA(A)-receptor mediated signaling, and stimulating the GABA(A) receptor can reverse the dysfunction of GABAergic inhibition in the motor circuits in the basal ganglia. (C) 2004 Elsevier Inc. All rights reserved.-
dc.languageEnglish-
dc.publisherACADEMIC PRESS INC ELSEVIER SCIENCE-
dc.subjectGENE-EXPRESSION-
dc.subjectBASAL GANGLIA-
dc.subjectSTRIATOPALLIDAL NEURONS-
dc.subjectLOCOMOTOR IMPAIRMENT-
dc.subjectSUBTHALAMIC NEURONS-
dc.subjectGABA(A) RECEPTORS-
dc.subjectRAT HIPPOCAMPUS-
dc.subjectPARS RETICULATA-
dc.subjectIN-VITRO-
dc.subjectNGFI-A-
dc.titleAltered GABAergic neurotransmission in mice lacking dopamine D2 receptors-
dc.typeArticle-
dc.identifier.doi10.1016/j.mcn.2003.12.010-
dc.description.journalClass1-
dc.identifier.bibliographicCitationMOLECULAR AND CELLULAR NEUROSCIENCE, v.25, no.4, pp.732 - 741-
dc.citation.titleMOLECULAR AND CELLULAR NEUROSCIENCE-
dc.citation.volume25-
dc.citation.number4-
dc.citation.startPage732-
dc.citation.endPage741-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.identifier.wosid000220852400016-
dc.identifier.scopusid2-s2.0-11144356288-
dc.relation.journalWebOfScienceCategoryNeurosciences-
dc.relation.journalResearchAreaNeurosciences & Neurology-
dc.type.docTypeArticle-
dc.subject.keywordPlusGENE-EXPRESSION-
dc.subject.keywordPlusBASAL GANGLIA-
dc.subject.keywordPlusSTRIATOPALLIDAL NEURONS-
dc.subject.keywordPlusLOCOMOTOR IMPAIRMENT-
dc.subject.keywordPlusSUBTHALAMIC NEURONS-
dc.subject.keywordPlusGABA(A) RECEPTORS-
dc.subject.keywordPlusRAT HIPPOCAMPUS-
dc.subject.keywordPlusPARS RETICULATA-
dc.subject.keywordPlusIN-VITRO-
dc.subject.keywordPlusNGFI-A-
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