Uptake and release for glutamine and glutamate in a crude synaptosomal fraction from rat brain.
[14C]Glutamine uptake in a crude synaptosomal (P2) fraction, (representing the sum of [14C]glutamine accumulated and [14C]glutamate formed by hydrolysis), is distinct from glutamate uptake. Glutamine uptake is Na+-independent and unaffected by the Na+-K+-ATPase inhibitor ouabain, whereas glutamate uptake is Na+-dependent and inhibited by ouabain. The uptake of both glutamine and glutamate is unaffected by the gamma-glutamyltransferase inhibitor, Acivicin. This indicates that glutamine uptake is not mediated by a carrier, as distinct from that of glutamate, and also not linked to gamma-glutamyl-transferase. Na+ affects the distribution of glutamine-derived glutamate by increasing the synaptosomal content and reducing that of the medium. When glutamate release from synaptosomes preloaded with [14C]glutamate is measured by superfusion technique in order to prevent reuptake, Na+ has been found to inhibit release in a non-depolarizing medium (Ringer buffer with no Ca2+) of the [14C]glutamate as well as of endogenous glutamate. The specific activity of the [14C]glutamine-derived glutamate in the incubation medium is much higher than that in the synaptosomes, indicating that there exists a readily releasable pool of newly formed glutamate in addition to another pool. The latter glutamate pool is partially reduced by Na+.
D000818:Animals; D001921:Brain / Q000378:metabolism*; D005971:Glutamates / Q000378:metabolism*; D018698:Glutamic Acid; D005973:Glutamine / Q000378:metabolism*; D010042:Ouabain / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D012964:Sodium / Q000502:physiology; D000254:Sodium-Potassium-Exchanging ATPase / Q000502:physiology; D013574:Synaptosomes / Q000378:metabolism
D005971:Glutamates; D005973:Glutamine; D018698:Glutamic Acid; D010042:Ouabain; D012964:Sodium; D000254:Sodium-Potassium-Exchanging ATPase