We studied the effect of glutamate, N -methyl- d -aspartate (NMDA), kainate or K + depolarization, on neurotoxicity in cultured chick retinal cells, under conditions in which we could discriminate between Ca 2− entering through ionotropic glutamate receptors and voltage-sensitive Ca 2+ channels (VSCCs). When neurons were challenged with NMDA, kainate or glutamate, in Na + -containing medium, a decrease in cell survival was observed, whereas K + depolarization did not affect the viability of the cells. The Mg 2+ ion completely prevented the toxic effect mediated by the NMDA receptor, and had a small but significant protective effect at the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid/kainate (AMPA/kainate) receptor-induced cell death. We observed that, in a Na + -free N -methyl- d -glucamine (NMG) medium, to avoid the activation of VSCCs indirectly by the glutamate receptor agonists, stimulation of the glutamate receptors causes Ca 2+ influx only through NMDA and AMPA/kainate receptor-associated channels, and that Ca 2+ entry correlates well with subsequent cell death. These results show that the activation of NMDA or AMPA/kainate receptors can cause excitotoxicity in retinal neurons by mechanisms not involving Na + influx, but rather depending on the permeation of Ca 2+ through glutamate receptor-associated channels. For small Ca 2+ loads the entry of Ca 2+ through the NMDA receptor-associated channel was more efficient in triggering cell death than the influx of Ca 2+ through the AMPA/kainate receptor.
European Journal of Pharmacology – Elsevier
Published: Apr 29, 1996
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