Abstract
Excitatory amino acids such as L-glutamate (Glu) and quisqualate (QUIS) markedly potentiated K+-evoked release of exogenous [3H]dopamine (DA) from rat striatal slices. Intrastriatal kainic acid injections resulted in a total disappearance of the stimulatory effects of Glu on evoked-release of [3H]DA as well as in a parallel reduction in the maximal number (Bmax) of a D-aspartate-insensitive L-[3H]Glu binding site in striatal particulate fractions. Following cortical ablation, the potentiating effect of Glu on [3H]DA release in decorticated striatal slices lasted longer, compared to normal slices, and occurred during the 2nd min following K+-depolarization. However, the extent (%) of Glu stimulation on [3H]DA release remained the same in decorticated and normal striatal slices. Cortical ablation produced also a significant decrease in the Bmax and in the KD' of the D-aspartate-insensitive binding site towards L-[3H]Glu. These results support the proposal that the D-aspartate-insensitive Glu binding site is somehow related to an amino acid receptor-mediated modulation of dopaminergic transmission in the rat corpus striatum.
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