Both repeated restraint stress and MAFP prolong DSI; if there is a shared mechanism subserving this prolongation we would expect that MAFP and repeated restraint stress would produce a mutually occlusive enhancement of DSI. We therefore tested DSI in mice exposed to 10 days of restraint stress in the presence of MAFP (1 µM). Two-way ANOVA showed a significant effect of time (p < 0.0001), stress (p < 0.0001), but no significant interaction (p < 0.05; Figure 6c). Summary data indicate maximal DSI was not different between repeated restraint stress (74.0 ± 4.8% N = 18), control-MAFP (66.3 ± 5.4% N = 8), and repeated restraint stress-MAFP (67.8 ± 4.4% N = 6) groups, p > 0.05 for all comparisons (Figure 6d). Late DSI was also not different between repeated restraint stress (80.2 ± 3.8% N = 18), control-MAFP (74.7 ± 3.6% N = 8), and repeated restraint stress-MAFP (80.0 ± 7.4 N = 6 groups), p > 0.05 for all comparisons (Figure 6d). These data suggest a mechanism involving impaired 2-AG degradation could subserve the prolongation of DSI observed after repeated stress exposure.
