| First Author | Wang SE | Year | 2017 |
| Journal | Cell Rep | Volume | 19 |
| Issue | 2 | Pages | 401-412 |
| PubMed ID | 28402861 | Mgi Jnum | J:250764 |
| Mgi Id | MGI:6103215 | Doi | 10.1016/j.celrep.2017.03.050 |
| Citation | Wang SE, et al. (2017) TRPV1 Regulates Stress Responses through HDAC2. Cell Rep 19(2):401-412 |
| abstractText | 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. |
