Abstract

We examined the properties of voltage-gated calcium channels mediating endogenous dopamine (DA) and acetylcholine (ACh) release in the isolated rat retina. Application of 30 mM KCl elicited the release of DA and ACh, and these releases were abolished in Ca 2+-free medium. The high K +-evoked DA release was largely blocked by both of ω-agatoxin IVA and ω-conotoxin MVIIC, P- and Q-type calcium channel antagonists, and partly blocked by isradipine, an L-type calcium channel antagonist, and ω-conotoxin GVIA, an N-type calcium channel antagonist, ω-Agatoxin IVA at a small dose, sufficient to block P-type channels alone, was however without effect. On the other hand, the high K +-evoked ACh release was partly blocked by ω-agatoxin IVA and ω-conotoxin MVIIC, but was resistant to isradipine and ω-conotoxin GVIA. Flunarizine, a non-selective T-type calcium channel antagonist, did not inhibit the release of DA and ACh. Cd 2+ markedly blocked the release of both DA and ACh, Co 2+ and Ni 2+ slightly blocked the release of DA, and the release of ACh was not blocked by these two divalent cations. These results suggest that the high K +-evoked release of retinal DA is largely mediated by ω-agatoxin IVA and ω-conotoxin MVIIC sensitive calcium channels (probably Q-type channels), while the release of retinal ACh is largely mediated by as yet uncharacterized Cd 2+ sensitive calcium channels. The properties of voltage-gated calcium channels involved in the release of ACh in the rat retina differ from those of DA.

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