Differences in the release of L-glutamate and D-aspartate from primary neuronal chick cultures

Abstract

Primary neuronal cultures were made from eight-day-old embryonic chick telencephalon. Ten-day-old cultures were used to study the release of D-[3H]aspartate and L-[3H]glutamate. The D[3H]aspartate release was stimulated by increasing potassium concentrations, but it was not calcium dependent. In contrast, the potassium dependent L-[3H]glutamate release was calcium dependent, and furthermore L-[3H]glutamate release was optimal at potassium concentrations < 30 mM. The inhibitors of glutamate uptake, dihydrokainate and 1-aminocyclobutane-trans-1,3-dicarboxylic acid (CACB), also referred to as cis-1 -aminocyclobutane-1,3-dicarboxylate, were used in the release experiments. Dihydrokainate had no effect on aspartate release, whereas CACB increased both the basal efflux of D-[3H]aspartate and the potassium evoked release. CACB had no effect on the potassium stimulated L-glutamate release. We believe that L-glutamate is released mainly by a vesicular mechanism from the presumably glutamatergic neurons present in our culture. D-aspartate release observed by us, could be mediated by a transporter protein. The cellular origin of this release remains to be assessed.