Albrecht J
Department of Neuropathology, Medical Research Centre, Polish Academy of Sciences, Warsaw.
Neuropharmacology. 1989 Aug;28(8):885-7. doi: 10.1016/0028-3908(89)90183-4.
Bulk isolated rat astrocytes loaded with [14C] glutamine (Gln) were superfused on glass fiber filters with a standard Krebs-Henseleit medium until the basal efflux of the radioactivity became constant. The samples were then pulse-treated with: L-glutamate (Glu), gamma-aminobutyric acid (GABA), L-aspartate (Asp), cold Gln, or catecholamines, each at 0.5 mM concentration. Of the neurotransmitters tested, only Glu stimulated the efflux of radio-labelled Gln. The effect of Glu was sodium-dependent and was not mimicked by the Glu-receptor agonists: N-methyl-D-aspartate (NMDA), quisqualate (Quis) or kainate (KA), indicating a transport-mediated mechanism. Glu did not stimulate the efflux of newly taken up glutamine from either crude or purified brain synaptosomes, which is in keeping with the existing evidence that astrocytes function as a glutamine donor to other compartments of the central nervous system.