Dependence of photoreceptor glutamate release on a dihydropyridine-sensitive calcium channel

Abstract

A “reduced retina” preparation, consisting of the photoreceptor layer attached to the pigment epithelium in the eyecup, was used to study the pharmacology of the calcium channels controlling glutamate release by photoreceptors in Xenopus. Glutamate release was evoked either by dark adaptation or by superfusion with elevated (20 mM) potassium medium. Both darkness- and potassium-induced release were blocked by cadmium (200 μM). The N-type calcium channel blocker, ω-conotoxin GVIA (500 nM), the P-type calcium channel blocker, ω-agatoxin IVA (20 nM), and the P- and Q-type channel blocker ω-conotoxin MVIIC (1 μM) had no effect on glutamate release. In contrast, the dihydropyridines, nifedipine (10 μM) and nitrendipine (10 μM), which affect L-type calcium channels, blocked both darkness- and potassium-induced release. Bay K 8644 (10 μM), which promotes the open state of L-type calcium channels, enhanced glutamate release. These results indicate that photoreceptor glutamate release is controlled mainly by dihydropyridine-sensitive calcium channels. A dependence of glutamate release on L-type calcium channels also has been reported for depolarizing bipolar cells of a fish retina. Thus, it appears that non-inactivating L-type calcium channels are appropriate to mediate transmitter release in neurons whose physiological responses are sustained, graded potentials.