Striatal dopamine participates in glutamate-induced hydroxyl radical generation.

Using a microdialysis technique we showed that the exposure of the rat striatum to glutamate yields hydroxyl radicals and results in striatal damage. We postulated that dopamine release is enhanced by glutamate perfusion and that the enzymatic metabolism of dopamine may account for this hydroxyl radical formation. The inhibition of monoamine oxidases by i.p. co-administration of clorgy-line and deprenyl reduced hydroxyl radical production induced by glutamate perfusion, but significantly increased the striatal damage. Our results suggest that the enzymatic metabolism of dopamine participates in glutamate-induced hydroxyl radical generation but that other by-products of dopamine may be responsible for the aggravation of the striatal injury.