| Autor: |
Sung Eun Wang, Seung Yeon Ko, Sungsin Jo, Miyeon Choi, Seung Hoon Lee, Hye-Ryeong Jo, Jee Young Seo, Sang Hoon Lee, Yong-Seok Kim, Sung Jun Jung, Hyeon Son |
| Jazyk: |
angličtina |
| Rok vydání: |
2017 |
| Předmět: |
|
| Zdroj: |
Cell Reports, Vol 19, Iss 2, Pp 401-412 (2017) |
| Druh dokumentu: |
article |
| ISSN: |
2211-1247 |
| DOI: |
10.1016/j.celrep.2017.03.050 |
| Popis: |
Summary: 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. : Wang et al. show that Trpv1−/− mice are more stress resilient than control mice following chronic unpredictable stress and these are associated with reduced histone deacetylase (HDAC) 2 expression and activity. As a consequence, HDAC2-regulated, cell-cycle- and neuroplasticity-related molecules are altered in Trpv1−/− mice. Their findings indicate that HDAC2 is a molecular link between TRPV1 activity and stress responses. Keywords: TRPV1, behavior, depression, stress, HDAC2, GR, hippocampus |
| Databáze: |
Directory of Open Access Journals |
| Externí odkaz: |
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