Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 손현 | - |
dc.date.accessioned | 2019-11-24T15:20:11Z | - |
dc.date.available | 2019-11-24T15:20:11Z | - |
dc.date.issued | 2017-04 | - |
dc.identifier.citation | CELL REPORTS, v. 19, no. 2, page. 401-412 | en_US |
dc.identifier.issn | 2211-1247 | - |
dc.identifier.uri | https://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.uri | https://repository.hanyang.ac.kr/handle/20.500.11754/113723 | - |
dc.description.abstract | Stress 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.sponsorship | This 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.iso | en_US | en_US |
dc.publisher | CELL PRESS | en_US |
dc.subject | MEDIATED GENE-TRANSCRIPTION | en_US |
dc.subject | GLUCOCORTICOID-RECEPTOR | en_US |
dc.subject | DENTATE GYRUS | en_US |
dc.subject | HIPPOCAMPAL NEUROGENESIS | en_US |
dc.subject | ENDOCANNABINOID SYSTEM | en_US |
dc.subject | PSYCHIATRIC-DISORDERS | en_US |
dc.subject | SYNAPTIC PLASTICITY | en_US |
dc.subject | CAPSAICIN RECEPTOR | en_US |
dc.subject | BEHAVIORAL DESPAIR | en_US |
dc.subject | MEMORY FORMATION | en_US |
dc.title | TRPV1 Regulates Stress Responses through HDAC2 | en_US |
dc.type | Article | en_US |
dc.relation.no | 2 | - |
dc.relation.volume | 19 | - |
dc.identifier.doi | 10.1016/j.celrep.2017.03.050 | - |
dc.relation.page | 401-412 | - |
dc.relation.journal | CELL REPORTS | - |
dc.contributor.googleauthor | Wang, Sung Eun | - |
dc.contributor.googleauthor | Ko, Seung Yeon | - |
dc.contributor.googleauthor | Jo, Sungsin | - |
dc.contributor.googleauthor | Choi, Miyeon | - |
dc.contributor.googleauthor | Lee, Seung Hoon | - |
dc.contributor.googleauthor | Jo, Hye-Ryeong | - |
dc.contributor.googleauthor | Seo, Jee Young | - |
dc.contributor.googleauthor | Lee, Sang Hoon | - |
dc.contributor.googleauthor | Kim, Yong-Seok | - |
dc.contributor.googleauthor | Jung, Sung Jun | - |
dc.relation.code | 2017009407 | - |
dc.sector.campus | S | - |
dc.sector.daehak | COLLEGE OF MEDICINE[S] | - |
dc.sector.department | DEPARTMENT OF MEDICINE | - |
dc.identifier.pid | hyeonson | - |
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.