D-aspartate release from cerebellar astrocytes: modulation of the high K-induced release by neurotransmitter amino acids.
The properties of D-aspartate release were studied in cerebellar astrocytes (14-15 DIV) in primary cultures in the rat. The spontaneous release of D-aspartate from astrocytes was fast, being further enhanced in Na- and Ca-free (EDTA-containing) media. Kainate, quisqualate, D-aspartate and L-glutamate stimulated the release, whereas L-glutamatediethylester was inhibitory. The release was enhanced by veratridine and high K (50 mM). Substitution of chloride by acetate in the experimental medium did not change the basal release but slightly decreased the potassium-induced release, indicating that the high K-induced D-aspartate release is primarily due to depolarization of cells. The K-stimulated release was independent of extracellular Ca2+ and potentiated by kainate and quisqualate. The effect of kainate was reduced by kynurenate, and that of quisqualate by L-glutamatediethylester. Glycine, taurine and GABA were equally effective in depressing the stimulated release of D-aspartate. The inhibition of GABA could be blocked by GABA antagonists. The results suggest that inhibitory amino acids may be involved in the regulation of glutamate release from cerebellar astrocytes. A further implication is that cerebellar astrocytes possess functional glutamate receptors of kainate and quisqualate subtypes.
Holopainen
I
I
Department of Biomedical Sciences, University of Tampere, Finland.
Kontro
P
P
D000596:Amino Acids / Q000378:metabolism* / Q000494:pharmacology; D000818:Animals; D000831:Animals, Newborn / Q000502:physiology; D001224:Aspartic Acid / Q000378:metabolism*; D001253:Astrocytes / Q000378:metabolism*; D002531:Cerebellum / Q000166:cytology / Q000378:metabolism*; D018377:Neurotransmitter Agents / Q000378:metabolism*; D011188:Potassium / Q000494:pharmacology*; D051381:Rats; D011919:Rats, Inbred Strains
D000596:Amino Acids; D018377:Neurotransmitter Agents; D001224:Aspartic Acid; D011188:Potassium