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-[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.
Lewin
L
L
Department of Cellular and Developmental Biology, Umeå University, Sweden.
Mattsson
M O
MO
Sellström
A
A
D000818:Animals; D001224:Aspartic Acid / Q000378:metabolism*; D001692:Biological Transport / Q000187:drug effects; D002478:Cells, Cultured; D002642:Chick Embryo; D004353:Drug Evaluation, Preclinical; D005089:Exocytosis / Q000187:drug effects; D005971:Glutamates / Q000494:pharmacology; D018698:Glutamic Acid / Q000378:metabolism*; D007608:Kainic Acid / Q000031:analogs & derivatives / Q000494:pharmacology; D009474:Neurons / Q000378:metabolism*
D005971:Glutamates; C066302:2,4-methanoglutamate; D001224:Aspartic Acid; D018698:Glutamic Acid; C020889:dihydrokainic acid; D007608:Kainic Acid