Figure 1. 8-CPT facilitated DSI by activating Epac2 in VTA dopamine neurons. A, In Epac+/+ slices, depolarization (from −70 to 0 mV, 5 s) did not induce DSI with control internal solution. Intracellular loading of 8-CPT (100 μm) enabled DSI (n = 8–9, p = 0.031). The 8-CPT-enabled DSI was blocked by the CB1 receptor antagonist AM251 (n = 7, p = 0.040). Sample traces of evoked IPSCs were shown on the top and averaged DSI on the bottom. The solid lines are single exponential fitting curves of the decay of DSI. B, DSI was not induced in Epac−/− slices with control internal solution or 8-CPT-containing internal solution (n = 8–10, p = 0.323). C, In Epac1−/− slices, 8-CPT enabled DSI (both n = 8, p < 0.001). D, DSI was not induced in Epac2−/− slices with control or 8-CPT-containing internal solution (n = 8–9, p = 0.760). E, DSI was not induced in Epac+/+ slices with control or 6-Bnz-cAMP-containing internal solution (n = 8–9, p = 0.101). F, Dose-dependent effects of intracellular loading of different concentrations of 8-CPT (n = 7–10, *p < 0.05, **p < 0.01).