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 striata l damage. We postulated that dopamine release is enhanced by glutamate perfusion and that the enzymatic metabolism of dopamine may account f or this hydroxyl radical formation. The inhibition of monoamine oxidas es by i.p. co-administration of clorgyl-line and deprenyl reduced hydr oxyl radical production induced by glutamate perfusion, but significan tly increased the striatal damage. Our results suggest that the enzyma tic metabolism of dopamine participates in glutamate-induced hydroxyl radical generation but that other by-products of dopamine may be respo nsible for the aggravation of the striatal injury.