RELEASE OF D-[H-3] ASPARTIC ACID FROM THE RAT SUBSTANTIA NIGRA - EFFECT OF VERATRIDINE-EVOKED DEPOLARIZATION AND CORTICAL ABLATION
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Date
1985
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Abstract
The spontaneous and veratridine-evoked release of radioactive D-aspartic acid, previously taken up by rat substantia nigra slices, was studied by using a superfusion system. Veratridine (25 .mu.M, 1 min) markedly produced a 14-fold increase in D-[3H]aspartic acid release from nigral slices. Omission of Ca2+ and increasing Mg2+ concentration to 12 mM in the superfusion medium did substantially block D-[3H]aspartate release induced by veratridine depolarization. Veratridine was able to evoke [3H]amino acid release which seemed to be, at least, 30% Ca2+-independent. Tetrodotoxin (0.01-0.1 .mu.M), a blocker of voltage-dependent Na+ channels, totally abolished veratridine-evoked release of D-[3H]aspartate from nigral slices. Lesion studies were performed to learn about the nature of the neuronal compartment in the substantia nigra upon which veratridine-depolarization acted to induce D-[3H]aspartate release. Unilateral ablation of the fronto-parietal cortex was accompanied by a significant decrease in the accumulation of nigral D-[3H]aspartate and by a large loss from ipsilateral nigral slices in D-[3H]aspartate release evoked by veratridine. Both the accumulation and veratridine-evoked release of [3H]dopamine, remained unchanged in the ipsilateral substantia nigra slices to the lesion. D-[3H]aspartic acid may be taken up and then released, in a Ca2+-dependent manner, by nerve terminals located in the substantia nigra. L-glutamate and/or L-aspartate may act as neurotransmitters at the cortico-nigral neuronal pathway.