Fig. 2.

UCMS leads to WM deficits associated with increased plasma corticosterone response and decreased pCREB immunoreactivity. (A) Experimental design: plasma corticosterone and number of pCREB-positive neurons were measured in the remaining UCMS and non-stressed (NS) mice sacrificed 30min after the beginning of WM testing (UCMS: N = 10; NS: N = 8) in the T-maze alternation task. (B); Left: Mean percentage of alternation rates were measured in Block A (Trials 2–4) and Block B (Trials 5–7) with a 90-sec inter-trial interval (ITI). Right:trial 8 had a shorter 5-sec ITI. (C)UCMS exposure significantly enhanced plasma corticosterone (ng/ml) under baseline condition (NAIVE) and after WM (TEST). (D) The numbers of positive pCREB nuclei/mm²were measured in the PFC, the dCA1 and the vCA1. In the NAÏVE groups, the UCMS mice had significantly higher pCREB-positive neurons in the PFC and the dCA1 compared to NS mice. WM testing induced significantly higher pCREB-positive neurons in both structures of the NS, but not of the UCMS mice. No effect of TEST nor UCMS was found in the vCA1. (E) Representative photomicrographs showing pCREB immunoreactivity in the PFC of NS (top) and UCMS (bottom) mice from the NAIVE (left) and TEST (right) groups. Bars represent means ± SEM.*P < 0.05, **P < 0.01 and ***P < 0.001 relative to the NS. P < 0.001 relative to the NAIVE.