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

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Abstract
Accumulation of L-.alpha.-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 .times. 10-4 M for the high-affinity system. D-.alpha.-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-.alpha.-aminoadipate. D- and L-.alpha.-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-.alpha.-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 2 compounds. Less than 10% of the preloaded D- and L-.alpha.-aminoadipate are metabolized by the cerebral cortex during 40 min of superfusion. The possibility of L-.alpha.-aminoadipate as a neurotransmitter candidate is discussed.

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