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TRPV1 Activation in Primary Cortical Neurons Induces Calcium-Dependent Programmed Cell Death

DC FieldValueLanguage
dc.contributor.author박경아-
dc.contributor.author송주현-
dc.contributor.author이원택-
dc.contributor.author이종은-
dc.contributor.author이준홍-
dc.date.accessioned2014-12-18T08:38:47Z-
dc.date.available2014-12-18T08:38:47Z-
dc.date.issued2013-
dc.identifier.issn1226-2560-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/86693-
dc.description.abstractTransient receptor potential cation channel, subfamily V, member 1 (TRPV1, also known as vanilloid receptor 1) is a receptor that detects capsaicin, a pungent component of chili peppers, and noxious heat. Although its function in the primary nociceptor as a pain receptor is well established, whether TRPV1 is expressed in the brain is still under debate. In this study, the responses of primary cortical neurons were investigated. Here, we report that 1) capsaicin induces caspase-3-dependent programmed cell death, which coincides with increased production of nitric oxide and peroxynitrite ; that 2) the prolonged capsaicin treatment induces a steady increase in the degree of capase-3 activation, which is prevented by the removal of capsaicin; 3) and that blocking calcium entry and calcium-mediated signaling prevents capsaicin-induced cell death. These results indicate that cortical neurons express TRPV1 whose prolonged activation causes cell death.-
dc.description.statementOfResponsibilityopen-
dc.relation.isPartOfExperimental Neurobiology-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.titleTRPV1 Activation in Primary Cortical Neurons Induces Calcium-Dependent Programmed Cell Death-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Neurology (신경과학)-
dc.contributor.googleauthorJuhyun Song-
dc.contributor.googleauthorJun Hong Lee-
dc.contributor.googleauthorSung Ho Lee-
dc.contributor.googleauthorKyung Ah Park-
dc.contributor.googleauthorWon Taek Lee-
dc.contributor.googleauthorJong Eun Lee-
dc.identifier.doi10.5607/en.2013.22.1.51-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA01424-
dc.contributor.localIdA02063-
dc.contributor.localIdA03007-
dc.contributor.localIdA03182-
dc.contributor.localIdA03146-
dc.relation.journalcodeJ00872-
dc.contributor.alternativeNamePark, Kyung Ah-
dc.contributor.alternativeNameSong, Ju Hyun-
dc.contributor.alternativeNameLee, Won Taek-
dc.contributor.alternativeNameLee, Jong Eun-
dc.contributor.alternativeNameLee, Jun Hong-
dc.contributor.affiliatedAuthorPark, Kyung Ah-
dc.contributor.affiliatedAuthorSong, Ju Hyun-
dc.contributor.affiliatedAuthorLee, Won Taek-
dc.contributor.affiliatedAuthorLee, Jun Hong-
dc.contributor.affiliatedAuthorLee, Jong Eun-
dc.rights.accessRightsfree-
dc.citation.volume22-
dc.citation.number1-
dc.citation.startPage51-
dc.citation.endPage57-
dc.identifier.bibliographicCitationExperimental Neurobiology, Vol.22(1) : 51-57, 2013-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Neurology (신경과학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Anatomy (해부학교실) > 1. Journal Papers

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