= 0.007; SDPS prone, t(9) = −3.59; P = 0.006; and SDPS resilient, t(9) = −2.70; P = 0.024 (Figure 5C). Notably, a main group effect was observed, repeated measures ANOVA: F GROUP(1, 32) = 3.74, P = 0.035, which was due to increased relapse in SDPS‐prone animals vs control (P = 0.011) and a trend vs SDPS‐resilient (P = 0.072) groups. The two latter groups performed almost identical (P = 0.520). Analysis of relapse performance alone confirmed that SDPS vulnerability triggered increased reinstatement of alcohol seeking (one‐way ANOVA SDPS prone, post hoc: P = 0.031 vs controls; P = 0.092 vs SDPS‐resilient group; and controls vs. SDPS resilient, P = 0.730). In agreement with our previous observation,20 pretreatment with guanfacine blocked reinstatement of alcohol seeking in all three groups: controls, t(14) = −0.03; P = 0.973; SDPS prone, t(9) = −0.15; P = 0.886; and SDPS resilient, t(9) = 1.00; P = 0.344 vs own extinction performance (Figure 5C). Importantly, guanfacine prevented increased reinstatement in the SDPS‐prone subpopulation, and between‐group differences were no longer observed, F GROUP(2, 32) = 2.07, P = 0.142 (Figure 5C). Taken together, relapse data pointed to an SDPS‐induced facilitation of reinstatement of alcohol seeking,
