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TRPV1 Regulates Stress Responses through HDAC2

Title
TRPV1 Regulates Stress Responses through HDAC2
Author
손현
Keywords
MEDIATED GENE-TRANSCRIPTION; GLUCOCORTICOID-RECEPTOR; DENTATE GYRUS; HIPPOCAMPAL NEUROGENESIS; ENDOCANNABINOID SYSTEM; PSYCHIATRIC-DISORDERS; SYNAPTIC PLASTICITY; CAPSAICIN RECEPTOR; BEHAVIORAL DESPAIR; MEMORY FORMATION
Issue Date
2017-04
Publisher
CELL PRESS
Citation
CELL REPORTS, v. 19, no. 2, page. 401-412
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.
URI
https://www.cell.com/cell-reports/fulltext/S2211-1247(17)30396-0?_returnURL=https%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS2211124717303960%3Fshowall%3Dtruehttps://repository.hanyang.ac.kr/handle/20.500.11754/113723
ISSN
2211-1247
DOI
10.1016/j.celrep.2017.03.050
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COLLEGE OF MEDICINE[S](의과대학) > MEDICINE(의학과) > Articles
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