Characterization of the N-methyl-d-aspartate (NMDA) receptor in the embryonic chick brain
The effect of oxidative stress, induced by ascorbate (1.5 mM)/Fe2+ (7.5 microM), on the cellular responses to N-methyl-D-aspartate (NMDA) receptor activation was evaluated by measuring the release of [3H]GABA induced by NMDA from cultured retina cells. In retina cells submitted to oxidative stress the [3H]GABA release evoked by NMDA, in a medium containing physiological concentrations of Mg2+ (1.6 mM) and K+ (4 mM), was significantly higher than in control cells. The [3H]GABA release evoked by NMDA was potentiated by glycine and was abolished by MK-801, suggesting that the [3H]GABA release was due to NMDA receptor activation. The increased effect of NMDA in peroxidized cells was significantly reduced by TTX, suggesting that the higher cellular responses to the activation of NMDA receptors are due to a hyperexcitability of retina cells submitted to oxidative stress. No significant differences were found between the average resting membrane potential of control and peroxidized cells. However, membrane potential is more tightly regulated by K(+)-channels sensitive to 4-aminopyridine (100 microM), alpha-dendrotoxin (100 nM) and gamma-dendrotoxin (100 nM) under oxidative stress.