Fig. 4.
Inhibition of stress-induced increased hdac1 expression promotes resilience and rescues cldn5 expression. (A) Following 10 d of CSDS, hdac1 expression is down-regulated in the NAc endothelial cells of RES mice when compared to SS mice (one-way ANOVA, *P = 0.0301, n = 4 to 5 mice/group). (B and C) Higher stress-induced hdac1 level in the NAc of SS mice was confirmed by quantitative PCR and negatively correlated with SI (SI ratio: one-way ANOVA: F2,34 = 44.27; ***P < 0.0001; hdac1 fold change: one-way ANOVA: F2,29 = 6.122; **P = 0.0061, Pearson’s correlation between SI ratio and hdac1 fold change: **P = 0.0068, n = 10 to 16 mice/group). (D) Mice were screened with the SI test following 10 d of CSDS and split equally in two groups then administered vehicle or MS-275. (E) A second SI test was performed after 10 d of treatment revealing increased social interactions in the MS-275–treated group (unpaired t test: ***P < 0.0001) in line with higher cldn5 expression (Pearson’s correlation: **P = 0.0019, n = 11 mice/group). One-way ANOVAs statistical test were significant, thus Bonferroni posttests were performed with **P < 0.01; ***P < 0.001.