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dc.contributor.author조성신-
dc.date.accessioned2019-11-24T16:23:23Z-
dc.date.available2019-11-24T16:23:23Z-
dc.date.issued2017-04-
dc.identifier.citationCELL REPORTS, v. 19, no. 2, page. 401-412en_US
dc.identifier.issn2211-1247-
dc.identifier.urihttps://www.cell.com/cell-reports/fulltext/S2211-1247(17)30396-0?_returnURL=https%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS2211124717303960%3Fshowall%3Dtrue-
dc.identifier.urihttps://repository.hanyang.ac.kr/handle/20.500.11754/113729-
dc.description.abstractStress causes changes in neurotransmission in the brain, thereby influencing stress-induced behaviors. However, it is unclear how neurotransmission systems orchestrate stress responses at the molecular and cellular levels. Transient receptor potential vanilloid 1 (TRPV1), a non-selective cation channel involved mainly in pain sensation, affects mood and neuroplasticity in the brain, where its role is poorly understood. Here, we show that Trpv1-deficient (Trpv1(-/-)) mice are more stress resilient than control mice after chronic unpredictable stress. We also found that glucocorticoid receptor (GR)-mediated histone deacetylase 2 (HDAC) 2 expression and activity are reduced in the Trpv1(-/-) mice and that HDAC2-regulated, cell-cycle- and neuroplasticity-related molecules are altered. Hippocampal knockdown of TRPV1 had similar effects, and its behavioral effects were blocked by HDAC2 overexpression. Collectively, our findings indicate that HDAC2 is a molecular link between TRPV1 activity and stress responses.en_US
dc.description.sponsorshipThis research was supported by National Research Foundation of Korea (NRF) grants funded by the Ministry of Education, Science and Technology (MEST), Republic of Korea (2011-0028317 and 2016R1A2B2006474; H.S.) and the Pioneer Research Center Program of the Ministry of Science, ICT and Future Planning (2011-0027921; S.J.J.).en_US
dc.language.isoen_USen_US
dc.publisherCELL PRESSen_US
dc.subjectMEDIATED GENE-TRANSCRIPTIONen_US
dc.subjectGLUCOCORTICOID-RECEPTORen_US
dc.subjectDENTATE GYRUSen_US
dc.subjectHIPPOCAMPAL NEUROGENESISen_US
dc.subjectENDOCANNABINOID SYSTEMen_US
dc.subjectPSYCHIATRIC-DISORDERSen_US
dc.subjectSYNAPTIC PLASTICITYen_US
dc.subjectCAPSAICIN RECEPTORen_US
dc.subjectBEHAVIORAL DESPAIRen_US
dc.subjectMEMORY FORMATIONen_US
dc.titleTRPV1 Regulates Stress Responses through HDAC2en_US
dc.typeArticleen_US
dc.identifier.doi10.1016/j.celrep.2017.03.050-
dc.relation.page401-412-
dc.relation.journalCELL REPORTS-
dc.contributor.googleauthorWang, Sung Eun-
dc.contributor.googleauthorKo, Seung Yeon-
dc.contributor.googleauthorJo, Sungsin-
dc.contributor.googleauthorChoi, Miyeon-
dc.contributor.googleauthorLee, Seung Hoon-
dc.contributor.googleauthorJo, Hye-Ryeong-
dc.contributor.googleauthorSeo, Jee Young-
dc.contributor.googleauthorLee, Sang Hoon-
dc.contributor.googleauthorKim, Yong-Seok-
dc.contributor.googleauthorJung, Sung Jun-
dc.relation.code2017009407-
dc.sector.campusS-
dc.sector.daehakRESEARCH INSTITUTE[S]-
dc.sector.departmentRHEUMATISM CENTER-
dc.identifier.pidjoejo0517-
dc.identifier.orcidhttp://orcid.org/0000-0003-3034-5029-


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