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- W2607312902 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." @default.
- W2607312902 created "2017-04-28" @default.
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- W2607312902 date "2017-04-01" @default.
- W2607312902 modified "2023-09-30" @default.
- W2607312902 title "TRPV1 Regulates Stress Responses through HDAC2" @default.
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- W2607312902 doi "https://doi.org/10.1016/j.celrep.2017.03.050" @default.
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