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dc.contributor.authorChoi, S.-
dc.contributor.authorNa, H. S.-
dc.contributor.authorKim, J.-
dc.contributor.authorLee, J.-
dc.contributor.authorLee, S.-
dc.contributor.authorKim, D.-
dc.contributor.authorPark, J.-
dc.contributor.authorChen, C.-C.-
dc.contributor.authorCampbell, K. P.-
dc.contributor.authorShin, H.-S.-
dc.date.accessioned2024-01-21T01:00:30Z-
dc.date.available2024-01-21T01:00:30Z-
dc.date.created2021-09-02-
dc.date.issued2007-07-
dc.identifier.issn1601-1848-
dc.identifier.urihttps://pubs.kist.re.kr/handle/201004/134299-
dc.description.abstractAlthough T-type Ca2+ channels are implicated in nociception, the function of specific subtypes has not been well defined. Here, we compared pain susceptibility in mice lacking Ca(V)3.2 subtype of T-type Ca2+ channels (Ca(V)3.2(-/-)) with wild-type littermates in various behavioral models of pain to explore the roles of Ca(V)3.2 in the processing of noxious stimuli in vivo. In acute mechanical, thermal and chemical pain tests, Ca(V)3.2(-/-) mice showed decreased pain responses compared to wild-type mice. Ca(V)3.2(-/-) mice also displayed attenuated pain responses to tonic noxious stimuli such as intraperitoneal injections of irritant agents and intradermal injections of formalin. In spinal nerve ligation-induced neuropathic pain, however, behavioral responses of Ca(V)3.2(-/-) mice were not different from those of wild-type mice. The present study reveals that the Ca(V)3.2 subtype of T-type Ca2+ channels are important in the peripheral processing of noxious signals, regardless of modality, duration or affected tissue type.-
dc.languageEnglish-
dc.publisherBLACKWELL PUBLISHING-
dc.subjectROOT GANGLION NEURONS-
dc.subjectCALCIUM-CHANNEL-
dc.subjectCA2+ CHANNELS-
dc.subjectNEUROPATHIC PAIN-
dc.subjectSENSORY NEURONS-
dc.subjectAFFERENT NEURONS-
dc.subjectREDOX MODULATION-
dc.subjectFORMALIN TEST-
dc.subjectGENE FAMILY-
dc.subjectEXPRESSION-
dc.titleAttenuated pain responses in mice lacking Ca(V)3.2 T-type channels-
dc.typeArticle-
dc.identifier.doi10.1111/j.1601-183X.2006.00268.x-
dc.description.journalClass1-
dc.identifier.bibliographicCitationGENES BRAIN AND BEHAVIOR, v.6, no.5, pp.425 - 431-
dc.citation.titleGENES BRAIN AND BEHAVIOR-
dc.citation.volume6-
dc.citation.number5-
dc.citation.startPage425-
dc.citation.endPage431-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.identifier.wosid000247667000003-
dc.identifier.scopusid2-s2.0-33947540792-
dc.relation.journalWebOfScienceCategoryBehavioral Sciences-
dc.relation.journalWebOfScienceCategoryNeurosciences-
dc.relation.journalResearchAreaBehavioral Sciences-
dc.relation.journalResearchAreaNeurosciences & Neurology-
dc.type.docTypeArticle-
dc.subject.keywordPlusROOT GANGLION NEURONS-
dc.subject.keywordPlusCALCIUM-CHANNEL-
dc.subject.keywordPlusCA2+ CHANNELS-
dc.subject.keywordPlusNEUROPATHIC PAIN-
dc.subject.keywordPlusSENSORY NEURONS-
dc.subject.keywordPlusAFFERENT NEURONS-
dc.subject.keywordPlusREDOX MODULATION-
dc.subject.keywordPlusFORMALIN TEST-
dc.subject.keywordPlusGENE FAMILY-
dc.subject.keywordPlusEXPRESSION-
dc.subject.keywordAuthorchemical pain-
dc.subject.keywordAuthormechanical pain-
dc.subject.keywordAuthorneuropathic pain-
dc.subject.keywordAuthorspinal nerve ligation ( SNL)-
dc.subject.keywordAuthorthermal pain-
dc.subject.keywordAuthortonic inflammatory pain-
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