TRPV1 Regulates Stress Responses through HDAC2open access
- Authors
- Wang, Sung Eun; Ko, Seung Yeon; Jo, Sungsin; Choi, Miyeon; Lee, Seung Hoon; Jo, Hye-Ryeong; Seo, Jee Young; Lee, Sang Hoon; Kim, Yong-Seok; Jung, Sung Jun; Son, Hyeon
- Issue Date
- Apr-2017
- Publisher
- CELL PRESS
- Keywords
- TRPV1; behavior; depression; stress; HDAC2; GR; hippocampus
- Citation
- CELL REPORTS, v.19, no.2, pp.401 - 412
- Indexed
- SCIE
SCOPUS
- Journal Title
- CELL REPORTS
- Volume
- 19
- Number
- 2
- Start Page
- 401
- End Page
- 412
- URI
- https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/152626
- DOI
- 10.1016/j.celrep.2017.03.050
- ISSN
- 2211-1247
- 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.
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Collections - 서울 의과대학 > 서울 생리학교실 > 1. Journal Articles
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