Potentiation by cadmium ion of ATP‐evoked dopamine release in rat phaeochromocytoma cells

The effects of cadmium ion (Cd 2+ ) on release of dopamine and on an inward current evoked by extracellular ATP were investigated in rat phaeochromocytoma PC12 cells. Cd 2+ (100 μ m ‐3 mM) potentiated the dopamine release evoked by 30 μ m ATP from the cells. Cd 2+ (100 μ m ) shifted the concentration‐response curve of ATP‐evoked dopamine release to the left without affecting the maximal response. Suramin (30 μ m ) completely abolished the dopamine release evoked by 30 μ m ATP but only partially inhibited the release evoked by 100 μ m ATP consistent with its role as a competitive antagonist. The response evoked by 30 μ m ATP in the presence of Cd 2+ (300 μ m ) was comparable to that observed with 100 μ m ATP alone; however, only the former was almost completely inhibited by suramin. Cd 2+ (100 μ m ) potentiated an inward current activated by 30 μ m ATP alone. A higher concentration of Cd 2+ (300 μ m ) had a smaller effect on amplitude potentiation but significantly prolonged the duration of the current. The time‐course of the ATP‐evoked dopamine release was investigated using a real‐time monitoring system for dopamine release. Although Cd 2+ (300 μ m ) had little effect on the time‐course of activation the ATP‐evoked dopamine release, it produced a long‐lasting dopamine release which slowly returned to the baseline. Taken together, these observations suggest that Cd 2+ enhances ATP‐evoked dopamine release by affecting P 2 ‐purinoceptor/channels. The enhancement may be attributed to a Cd 2+ ‐dependent increase in sensitivity to ATP.