Activation of ion channel‐linked glutamate receptors, especially N‐methyl‐d‐aspartate (NMDA) receptors, mediates the excitotoxic effects of glutamate upon central neurons. We examined the hypothesis that activation of group I metabotropic glutamate receptors (mGluRs) would increase NMDA receptor‐mediated cortical neuronal death. Addition of the selective group I mGluR agonists, dihydroxyphenylglycine (DHPG) or trans‐azetidine‐2,4‐dicarboxylic acid (t‐ADA) potentiated NMDA‐induced neuronal death, and application of the group I mGluR‐selective antagonist, aminoindan‐1,5‐dicarboxylic acid (AIDA), as well as the non‐selective antagonists methyl‐4‐carboxyphenylglycine (MCPG) or 4‐carboxyphenylglycine (4CPG) reduced NMDA‐ and kainate‐induced neuronal death in murine cortical cultures. The pro‐excitotoxic effect of group I mGluR activation may be mediated largely by enhancement of glutamate release, as DHPG potentiated high potassium‐stimulated glutamate release, and the protective effects of both AIDA and MCPG were abolished when NMDA and alpha‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazole proprionic acid (AMPA) receptors were blocked immediately after toxic NMDA receptor overstimulation. The present data support the possibility that antagonizing group I mGluRs may be a useful strategy for attenuating excitotoxic neuronal death in certain disease states.
European Journal of Neuroscience – Wiley
Published: Jan 1, 1998
Keywords: ; ; ; ;
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