Glutamate receptor agonists evoked Ca2+-dependent and Ca2+-independent release of 3Hd-Aspartate from cultured chick retina cells

摘要

We studied the release of 3Hd-aspartate evoked by glutamate receptor agonists from monolayer cultures of chick retina cells, and found that activation of the glutamate receptors can evoke both Ca2+-dependent and Ca2+-independent release of 3Hd-aspartate. In Ca2+-free (no added Ca2+) Na+medium, the agonists of the glutamate receptors induced the release of 3Hd-aspartate with the following rank order of potency: kainate>α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)∼N-methyl-d-aspartate (NMDA). In media containing 1 mM CaCl2the release of 3Hd-aspartate evoked by NMDA, kainate and AMPA was increased by about 112, 20 and 39, respectively, as compared to the release evoked by the same agonists in Ca2+-free medium. NMDA was the most potent agonist in stimulating the Ca2+-dependent release of 3Hd-aspartate, possibly by exocytosis, and AMPA was as potent as kainate. The Ca2+-dependent release of 3Hd-aspartate evoked by kainate was dependent on the influx of Ca2+through the receptor associated channel, as well as through the N- (ω-Conotoxin GVIA-sensitive) and L- (nitrendipine-sensitive)type voltage-sensitive Ca2+channels (VSCC). The exocytotic release of 3Hd-aspartate evoked by AMPA relied exclusively on Ca2+entry through the L-type VSCC, whereas the effect of NMDA was partially mediated by the influx of Ca2+through the receptor-associated channel, but not through L- or N-type VSCC. Thus, activation of these different glutamate receptors under physiological conditions is expected to cause the release of cytosolic and vesicular glutamate, and the routes of Ca2+entry modulating vesicular release may be selectively recrui