DIFFERENCES IN THE RELEASE OF L-GLUTAMATE AND D-ASPARTATE FROM PRIMARY NEURONAL CHICK CULTURES

Primary neuronal cultures were made from eight-day-old embryonic chick telencephalon. Ten-day-old cultures were used to study the release of D-[H-3]aspartate and L-[H-3]glutamate. The D-[H-3]aspartate release w as stimulated by increasing potassium concentrations, but it was not c alcium dependent. In contrast, the potassium dependent L-[H-3]glutamat e release was calcium dependent, and furthermore L-[H-3]glutamate rele ase was optimal at potassium concentrations < 30 mM. The inhibitors of glutamate uptake, dihydrokainate and 1-aminocyclobutane-trans-1,3-dic arboxylic 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-[H-3]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. Th e cellular origin of this release remains to be assessed.