Release of d-[(3)H]aspartic acid from the rat substantia nigra: effect of veratridine-evoked depolarization and cortical ablation.
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 ?M, 1 min) markedly produced a 14-fold increase in d-[(3)H]aspartic acid release from nigral slices. Omission of Ca(2+) and increasing Mg(2+) concentration to 12 mM in the superfusion medium did substantially block d-[(3)H]aspartate release induced by veratridine depolarization. Nevertheless, veratridine was able to evoke [(3)H]amino acid release which seemed to be, at least, 30% Ca(2+)-independent. Additional experiments showed that tetrodotoxin (0.01-0.1 ?M), a blocker of voltage-dependent Na(+) channels, totally abolished veratridine-evoked release of d-[(3)H]aspartate from nigral slices. Lesion studies were performed in order to learn about the nature of the neuronal compartment in the substantia nigra upon which veratridine-depolarization acted to induce d-[(3)H]aspartate release. Unilateral ablation of the fronto-parietal cortex was accompanied by a significant decrease in the accumulation of nigral d-[(3)H]aspartate and by a large loss from ipsilateral nigral slices in d-[(3)H]aspartate release evoked by veratridine. In contrast, both the accumulation and veratridine-evoked release of [(3)H]dopamine, remained unchanged in the ipsilateral substantia nigra slices to the lesion. The findings reported suggest that d-[(3)H]aspartic acid may be taken up and then released, in a Ca(2+)-dependent manner, by nerve terminals located in the substantia nigra. In addition, the results shown provide support to the view that l-glutamate and/or l-aspartate may act as neurotransmitters at the cortico-nigral neuronal pathway.
Abarca
J
J
Laboratory of Biochemical Pharmacology, Department of Cell Biology, Pontificia Universidad Católica de Chile, Santiago, Chile.
Bustos
G
G