Abstract
Dihydropyridine calcium channel antagonists block a prolonged or ‘L-type’ component of voltage-dependent Ca 2+ current in patch-clamp recordings of postnatal rat retinal ganglion cells. In the present study on these neurons, calcium channel antagonists were found at 500–1000 nM concentrations to attenuate the early rise in [Ca 2+] i and the subsequent toxic effects of exogenous glutamate, N-methyl- d-aspartate (NMDA), or an endogenous glutamate-related compound present in the retinal cultures. Previous data have shown that the neurotoxicity engendered by these agents can also be prevented by selective NMDA antagonists. The present observation raise the possibility, at least in this preparation, that activation of both voltage-dependent calcium channels and NMDA receptor-operated channels contribute to the injurious effects triggered by molecules binding to the NMDA receptor.
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