Fig. S2.
CUS increased the plasma levels of corticosterone, and caffeine, and A2AR blockade prevented this increase. Male mice (10 wk old) were subjected to a 3-wk period of CUS (Table S1). Three days later, animals were gently immobilized, and blood was collected from the tail vein. Animals were killed at 9:00 AM on the day of blood collection. Compared with control mice (ctr), CUS increased the plasma levels of corticosterone. This increase was prevented by the regular consumption of either caffeine (1 g/L) [CUS F(1,70) = 7.95; caffeine F(1,70) = 2.34; interaction F(1,70) = 4.36] (A) or the selective A2AR antagonist KW6002 (3 mg/kg) [CUS F(1,33) = 15.30; KW6002 F(1,33) = 6.78; interaction F(1,33) = 4.99] (B) and also was abrogated by the global deletion of A2AR (g-A2AR-KO) [CUS F(1,36) = 14.91; genotype F(1,36) = 1.50; interaction F(1,36) = 6.41] (C) or by the selective deletion of neuronal A2AR in fb-A2AR-KO mice [CUS F(1,32) = 16.79; genotype F(1,32) = 20.55; interaction F(1,32) = 4.56] (D). Data are shown as mean ± SEM of 7–19 mice per group. *P < 0.05 using two-way ANOVA followed by a Newman–Keuls post hoc test; ns, nonsignificant.