Ca 2+ influx through glutamate receptor-associated channels in retina cells correlates with neuronal cell death

Ca 2+ influx through glutamate receptor-associated channels in retina cells correlates with... 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. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png European Journal of Pharmacology Elsevier

Ca 2+ influx through glutamate receptor-associated channels in retina cells correlates with neuronal cell death

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Publisher
Elsevier
Copyright
Copyright © 1996 Elsevier Ltd
ISSN
0014-2999
DOI
10.1016/0014-2999(96)00044-1
Publisher site
See Article on Publisher Site

Abstract

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.

Journal

European Journal of PharmacologyElsevier

Published: Apr 29, 1996

References

  • Quisqualate- and kainate-activated channels in mouse central neurons in culture
    Asher, M.L.; Nowak, L.
  • 3 H- d -aspartate release from cerebellar granule neurons is differentially regulated by glutamate- and K + -stimulation
    Belhage, B.; Rehder, V.; Hansen, S.B.; Kater, S.B.; Schousboe, A.
  • The role of glutamate neurotoxicity in hypoxic-ischemic neuronal death
    Choi, D.W.; Rothman, S.M.
  • (Ca 2+ ) i regulation by glutamate receptor agonists in cultured chick retina cells
    Duarte, C.B.; Santos, P.F.; Carvalho, A.P.
  • Excitatory amino acid neurotoxicity in cultured retinal neurons: involvement of N -methyl- d -aspartate (NMDA) and non-NMDA receptors and effect of ganglioside GM1
    Facci, L.; Leon, A.; Skaper, S.D.
  • Dantrolene prevents glutamate cytotoxicity and Ca 2+ release from intracellular stores in cultured cerebral cortical neurons
    Frandsen, A.; Schousboe, A.
  • Calcium regulation of gene expression in neurons: the mode of entry matters
    Gallin, W.J.; Greenberg, M.E.
  • Permeation of calcium through excitatory amino acid receptor channels in cultured rat hippocampal neurons
    Iino, M.; Ozawa, S.; Tsuzuki, K.
  • Permeation and block of N -methyl- d -aspartic acid receptor channels by divalent cations in mouse cultured central neurons
    Mayer, M.L.; Westbrook, G.L.
  • Arachidonic acid inhibits uptake of glutamate and glutamine but not GABA in cultured cerebellar granule cells
    Yu, A.C.; Chan, P.H.; Fishman, R.A.

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