Abstract
The convulsant, 3-mercaptopropionic acid (100-1000 microM) enhanced potassium-evoked release of exogenous D-aspartate from slices of rat cerebral cortex and cerebellum, but not that from slices of hippocampus. Elevation of excitant amino acid release may contribute to the convulsant action of 3-mercaptopropionic acid. Unlike the convulsant barbiturate CHEB, 3-mercaptopropionic acid did not influence protoveratrine-stimulated release of D-aspartate and its action on potassium-evoked release appeared to be not dependent on calcium ion fluxes. Several other convulsants, including bemegride (200 microM), benzodiazepine Ro-5-3663 (100 M), nikethamide (500 microM), pentylenetetrazole (500 microM), and 4,6,6-trimethylcaprolactam (100 and 500 microM), and the glutamate decarboxylase inhibitor isoniazid (500 microM) failed to influence potassium-evoked release of D-aspartate.
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