Functional and biochemical characteristics of a putative quisqualate-type receptor in rat striatum: Effect of brain lesions

Abstract
Excitatory amino acids such asl-glutamate (Glu) and quisqualate (QUIS) markedly potentiated K+-evoked release of exogeneous [3H]dopamine (DA) from rat striatal slices. Intranstriatal 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 ad-aspartate-insensitivel-[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 occured 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 theK d' of thed-aspartateinsensitive binding site towardsl[3H]Glu. These results support the proposal that thed-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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