Figure 4.

CB1R-mediated effects at RBC terminals involve G-protein αi/o in a cAMP-dependent, but PKA-independent manner

(A) Representative traces (left) and summary graphs (right) showing that the G-protein βγ inhibitor Gallein (75 μM) had no effect on WIN-mediated decrease of sEPSC frequency and amplitude in AII ACs (n = 9 cells/4 animals).

(B) Blocking G-protein αi/o with the inhibitor NF-023 (10 μM) strongly decreased the sEPSC frequency and occluded the WIN-mediated decrease of sEPSC frequency and amplitude in AII ACs (n = 9 cells/4 animals).

(C) Bath application of the adenylyl cyclase activator forskolin (FSK, data pooled for 10 and 50 μM) had no effect on the sEPSC frequency or amplitude but eliminated the WIN-mediated decrease of sEPSC frequency and amplitude in AII ACs (n = 11 cells/7 animals).

(D) Bath application of PKA inhibitor H89 (10 μM) decreased the sEPSC amplitude but did not prevent the WIN-mediated decrease of sEPSC frequency and amplitude in AII ACs (n = 9 cells/6 animals). Data are presented as mean ± S.E.M and open circles represent a single cell. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001. Multiple comparisons were made using one-way ANOVA-RM, followed by a post-hoc Tukey test, or using Friedman ANOVA followed by a post-hoc WMNT test. For statistics, see Table S1.