1. The effects of cadmium ion (Cd2+) on release of dopamine and on an inward current evoked by extracellular ATP were investigated in rat phaeochromocytoma PC12 cells. 2. Cd2+ (100 μM-3 mM) potentiated the dopamine release evoked by 30 μM ATP from the cells. Cd2+ (100 μM) shifted the concentration-response curve of ATP-evoked dopamine release to the left without affecting the maximal response. 3. Suramin (30 μM) completely abolished the dopamine release evoked by 30 μM ATP but only partially inhibited the release evoked by 100 μM ATP consistent with its role as a competitive antagonist. The response evoked by 30 μM ATP in the presence of Cd2+ (300 μM) was comparable to that observed with 100 μM ATP alone; however, only the former was almost completely inhibited by suramin. 4. Cd2+ (100 μM) potentiated an inward current activated by 30 μM ATP alone. A higher concentration of Cd2+ (300 μM) had a smaller effect on amplitude potentiation but significantly prolonged the duration of the current. 5. The time-course of the ATP-evoked dopamine release was investigated using a real-time monitoring system for dopamine release. Although Cd2+ (300 μM) 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. 6. Taken together, these observations suggest that Cd2+ enhances ATP-evoked dopamine release by affecting P2-purinoceptor/channels. The enhancement may be attributed to a Cd2+-dependent increase in sensitivity to ATP.
|Number of pages||5|
|Journal||British Journal of Pharmacology|
|Publication status||Published - 1996|
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