Sodium and potassium ions and accumulation of labelled D-aspartate and GABA in crude synaptosomal fraction from rat cerebral cortex.

Abstract

Abstract—The accumulation of labelled d‐aspartate into crude synaptosomal fraction (P2) prepared from the rat cerebral cortex proceeded by a ‘high affinity’ system (Km= 15.1 μm The maximal velocity of d‐aspartate uptake was higher than that of the ‘high affinity’ component of l‐aspartate uptake and almost equal to that of l‐glutamate under the same incubation conditions. Negligible metabolism of labelled d‐aspartate was observed in the P2 fraction. These findings are in accord with those which have been reported for rat cerebral cortical slices. The following observations were made on d‐aspartate uptake into rat cerebral P2 fraction. (1) The requirement of sodium is almost absolute and obligatory. (2) The affinity of the carrier for the substrate is increased by increasing sodium concentration in the medium, but the maximal velocity is not altered. (3) It is suggested that sodium ion is co‐transported mole for mole with the substrate molecule. (4) Omission of potassium from the medium inhibits the uptake competitively. (5) Ouabain is a competitive inhibitor on the uptake. (6) Whereas thallium, rubidium and ammonium are efficient substitutes for potassium in exhibiting Na–K ATPase activity of the P2 fraction, the uptake is activated only by rubidium in the absence of potassium. These observations were in common with the uptake of l‐aspartate as well as of l‐ and d‐glutamate, but not with GABA uptake. The requirement of sodium for the uptake of d‐glutamate was indicated to be higher than that in the uptake of the other amino acids. Mutual inhibitions of the uptake among l‐ and d‐isomers of glutamate and aspartate suggested that a common carrier is involved in the transport. Mechanisms of the transport of these amino acids in the crude synaptosomal fraction were discussed.