Fig. 2.

Male SSTCre:γ2^f/fmice are resilient to chronic stress-induced increases in eEF2 phosphorylation in mPFC. A,B) UCMS increased p-eEF2^T56/eEF2 independent of sex and genotype in the ventral hippocampus (A) (F_{1, 102} = 6.22, p = 0.014) but not mPFC (B) (F_{1, 97} = 2.81, p = 0.10). C,D) Males: Representative western blots of male mice and summary statistics of p-eEF2^T56/eEF2 in ventral hippocampus and mPFC. In hippocampus (C), p-eEF2^T56/eEF2 showed a stress effect (F_{1, 51} = 5.93, p = 0.018). In mPFC (D), p-eEF2^T56/eEF2 showed an interaction of stress and genotype (F_1,41 = 8.63, p = 0.005). UCMS tended to increase p-eEF2^T56/eEF2 in γ2^f/f mice (p = 0.08, n = 9–14) but reduced this ratio in SSTCre:γ2^f/f mice (p = 0.02, n = 9–13). The p-eEF2^T56 level of UCMS γ2^f/f mice was increased compared to that of UCMS SSTCre:γ2^f/f mice (p = 0.02, n = 9).E,F) Females: In hippocampus (E), p-eEF2^T56/eEF2 showed an overall stress effect (F_1,47 = 7.90, p = 0.007) that was almost significant in γ2^f/f (p = 0.06) and significant in SSTCre:γ2^f/f mice (p = 0.046, n = 12–13). In mPFC (F), the p-eEF2^T56/eEF2 ratio showed stress (F_1,52 = 6.50, p = 0.014) and genotype effects (F_1,52 = 5.77, p = 0.020) and a stress × genotype interaction (F_1,52 = 9.16, p = 0.004). NS SSTCre:γ2^f/f mice vs. NS γ2^f/f controls showed a paradoxical reduction of p-eEF2^T56/eEF2 (p = 0.0003, n = 13–16). 2-way ANOVAs and Fisher's test. Graphs represent means ± SE. *p < 0.05, **p < 0.01, ***p < 0.001.