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dc.contributor.authorKim, Baeksun-
dc.contributor.authorIm, Heh-In-
dc.date.accessioned2024-01-19T14:34:09Z-
dc.date.available2024-01-19T14:34:09Z-
dc.date.created2022-01-25-
dc.date.issued2021-05-
dc.identifier.issn1355-6215-
dc.identifier.urihttps://pubs.kist.re.kr/handle/201004/117018-
dc.description.abstractNicotine can diversely affect neural activity and motor learning in animals. However, the impact of chronic nicotine on striatal activity in vivo and motor learning at long-term sparse timescale remains unknown. Here, we demonstrate that chronic nicotine persistently suppresses the activity of striatal fast-spiking parvalbumin interneurons, which mediate nicotine-induced deficit in sparse motor learning. Six weeks of longitudinal in vivo single-unit recording revealed that mice show reduced activity of fast-spiking interneurons in the dorsal striatum during chronic nicotine exposure and withdrawal. The reduced firing of fast-spiking interneurons was accompanied by spike broadening, diminished striatal delta oscillation power, and reduced sample entropy in local field potential. In addition, chronic nicotine withdrawal impaired motor learning with a weekly sparse training regimen but did not affect general locomotion and anxiety-like behavior. Lastly, the excitatory DREADD hM3Dq-mediated activation of striatal fast-spiking parvalbumin interneurons reversed the chronic nicotine withdrawal-induced deficit in sparse motor learning. Taken together, we identified that chronic nicotine withdrawal impairs sparse motor learning via disruption of activity in striatal fast-spiking parvalbumin interneurons. These findings suggest that sparse motor learning paradigm can reveal the subtle effect of nicotine withdrawal on motor function and that striatal fast-spiking parvalbumin interneurons are a neural substrate of nicotine's effect on motor learning.-
dc.languageEnglish-
dc.publisherTaylor & Francis-
dc.titleChronic nicotine impairs sparse motor learning via striatal fast-spiking parvalbumin interneurons-
dc.typeArticle-
dc.identifier.doi10.1111/adb.12956-
dc.description.journalClass1-
dc.identifier.bibliographicCitationAddiction Biology, v.26, no.3-
dc.citation.titleAddiction Biology-
dc.citation.volume26-
dc.citation.number3-
dc.description.isOpenAccessY-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.identifier.wosid000556212400001-
dc.identifier.scopusid2-s2.0-85089098451-
dc.relation.journalWebOfScienceCategoryBiochemistry & Molecular Biology-
dc.relation.journalWebOfScienceCategorySubstance Abuse-
dc.relation.journalResearchAreaBiochemistry & Molecular Biology-
dc.relation.journalResearchAreaSubstance Abuse-
dc.type.docTypeArticle-
dc.subject.keywordPlusANXIETY-LIKE BEHAVIOR-
dc.subject.keywordPlusDORSAL STRIATUM-
dc.subject.keywordPlusCHOLINERGIC INTERNEURONS-
dc.subject.keywordPlusPERFORMANCE IMPROVEMENT-
dc.subject.keywordPlusDIFFERENTIAL REGULATION-
dc.subject.keywordPlusSYNAPTIC PLASTICITY-
dc.subject.keywordPlusNEURAL INFORMATION-
dc.subject.keywordPlusDOPAMINE RELEASE-
dc.subject.keywordPlusSEX-DIFFERENCES-
dc.subject.keywordPlusSPATIAL MEMORY-
dc.subject.keywordAuthorlocal field potential-
dc.subject.keywordAuthormotor learning-
dc.subject.keywordAuthornicotine withdrawal-
dc.subject.keywordAuthordorsal striatum-
dc.subject.keywordAuthorextracellular single-unit recording-
dc.subject.keywordAuthorfast-spiking interneurons-
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