Glutamate and aspartate transport in rat brain mitochondria

Abstract

Rat brain mitochondria did not swell in iso osmotic solutions of ammonium or potassium (plus valinomycin) glutamate or aspartate, with or without addition of uncouplers. Glutamate was able to reduce intramitochondrial NAD(P)+; aspartate was able to cause partial reoxidation. These effects were inhibited by threo hydroxyaspartate in whole but not in lysed mitochondria. The existence of a 'malate aspartate shuttle' for the oxidation of extramitochondrial NADH was demonstrated. This shuttle requires the net exchange of glutamate for aspartate across the mitochondrial membrane. Extramitochondrial glutamate did not inhibit intramitochondrial glutaminase under conditions in which the inhibition in lysed mitochondria was virtually complete. The glutaminase activity of these mitochondria was not energy dependent. It is concluded that these mitochondria do not possess a glutamate hydroxyl antiporter similar to that of liver mitochondria nor a glutamate glutamine antiporter similar to that of pig kidney mitochondria, but that they do possess a glutamate aspartate antiporter.