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Uptake, Release, and Metabolism of D‐ and L‐α‐Aminoadipate by Rat Cerebral Cortex

Abstract: Accumulation of L‐α‐aminoadipate by rat cerebral cortical slices is a stereospecific and Na+‐dependent process. The uptake of this compound is also temperature‐dependent, with a Km, of 1.6 × 10−4M for the high‐affinity system. D‐α‐Aminoadipate has characteristics similar to those displayed by the L‐isomer but to a lesser degree. L‐Glutamate and L‐aspartate inhibit the uptake of L‐α‐aminoadipate. D‐ and L‐α‐Aminoadipate are, respectively, weak uncompetitive and weak competitive inhibitors for the uptake of L‐glutamate and L‐aspartate. Both enantiomers inhibit GABA uptake but in quite different ways. The release of L‐α‐aminoadipate from the cerebral cortical slices is stimulated by a high concentration of K+ ions in the presence of Ca2+ in the perfusion buffer; the D‐isomer displays this property to a lesser degree. The omission of Ca2+ markedly reduces the release of these two compounds. Less than 10% of the preloaded D‐ and L‐α‐aminoadipate are metabolized by the cerebral cortex during 40 min of superfusion. The possibility of L‐α‐aminoadipate as a neurotransmitter candidate is discussed.