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시냅스뇌질환연구단
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Hyperactive ACC-MDT Pathway Suppresses Prepulse Inhibition in Mice

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dc.contributor.authorYangsik Kim-
dc.contributor.authorNoh, Young Woo-
dc.contributor.authorKim, Kyungdeok-
dc.contributor.authorEunjoon Kim-
dc.date.accessioned2021-03-18T23:30:03Z-
dc.date.accessioned2021-03-18T23:30:03Z-
dc.date.available2021-03-18T23:30:03Z-
dc.date.available2021-03-18T23:30:03Z-
dc.date.created2021-02-26-
dc.date.issued2021-01-
dc.identifier.issn0586-7614-
dc.identifier.urihttps://pr.ibs.re.kr/handle/8788114/9215-
dc.description.abstractAltered prepulse inhibition (PPI) is an endophenotype associated with multiple brain disorders, including schizophrenia. Circuit mechanisms that regulate PPI have been suggested, but none has been demonstrated through direct manipulations. IRSp53 is an abundant excitatory postsynaptic scaffold implicated in schizophrenia, autism spectrum disorders, and attention-deficit/hyperactivity disorder. We found that mice lacking IRSp53 in cortical excitatory neurons display decreased PPI. IRSp53-mutant layer 6 cortical neurons in the anterior cingulate cortex (ACC) displayed decreased excitatory synaptic input but markedly increased neuronal excitability, which was associated with excessive excitatory synaptic input in downstream mediodorsal thalamic (MDT) neurons. Importantly, chemogenetic inhibition of mutant neurons projecting to MDT normalized the decreased PPI and increased excitatory synaptic input onto MDT neurons. In addition, chemogenetic activation of MDT-projecting layer 6 neurons in the ACC decreased PPI in wild-type mice. These results suggest that the hyperactive ACC-MDT pathway suppresses PPI in wild-type and IRSp53-mutant mice.-
dc.language영어-
dc.publisherOXFORD UNIV PRESS-
dc.titleHyperactive ACC-MDT Pathway Suppresses Prepulse Inhibition in Mice-
dc.typeArticle-
dc.type.rimsART-
dc.identifier.wosid000649368900008-
dc.identifier.scopusid2-s2.0-85100361774-
dc.identifier.rimsid74756-
dc.contributor.affiliatedAuthorYangsik Kim-
dc.contributor.affiliatedAuthorEunjoon Kim-
dc.identifier.doi10.1093/schbul/sbaa090-
dc.identifier.bibliographicCitationSCHIZOPHRENIA BULLETIN, v.47, no.1, pp.31 - 43-
dc.relation.isPartOfSCHIZOPHRENIA BULLETIN-
dc.citation.titleSCHIZOPHRENIA BULLETIN-
dc.citation.volume47-
dc.citation.number1-
dc.citation.startPage31-
dc.citation.endPage43-
dc.type.docTypeArticle-
dc.description.journalClass1-
dc.description.journalClass1-
dc.description.isOpenAccessN-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassssci-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaPsychiatry-
dc.relation.journalWebOfScienceCategoryPsychiatry-
dc.subject.keywordPlusDE-NOVO-
dc.subject.keywordPlusRAT-
dc.subject.keywordPlusORGANIZATION-
dc.subject.keywordPlusMEDIODORSAL THALAMIC NUCLEUS-
dc.subject.keywordPlusPREFRONTAL CORTEX-
dc.subject.keywordPlusGABAERGIC NEURONS-
dc.subject.keywordPlusDENDRITIC SPINES-
dc.subject.keywordPlusSTARTLE RESPONSE-
dc.subject.keywordPlusARP2/3 COMPLEX-
dc.subject.keywordPlusNEURAL CIRCUIT-
dc.subject.keywordAuthorprepulse inhibition-
dc.subject.keywordAuthormediodorsal thalamus-
dc.subject.keywordAuthorIRSp53-
dc.subject.keywordAuthorDREADD-
dc.subject.keywordAuthorschizophrenia-
dc.subject.keywordAuthoranterior cingulate cortex-
Appears in Collections:
Center for Synaptic Brain Dysfunctions(시냅스 뇌질환 연구단) > 1. Journal Papers (저널논문)
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