Uptake, Release, and Metabolism of D- and L-α-Aminoadipate by Rat Cerebral Cortex
Version of Record online: 5 OCT 2006
Journal of Neurochemistry
Volume 36, Issue 3, pages 1127–1136, March 1981
How to Cite
Charles, A. K. and Chang, Y.-F. (1981), Uptake, Release, and Metabolism of D- and L-α-Aminoadipate by Rat Cerebral Cortex. Journal of Neurochemistry, 36: 1127–1136. doi: 10.1111/j.1471-4159.1981.tb01709.x
- Issue online: 5 OCT 2006
- Version of Record online: 5 OCT 2006
- Received June 6, 1980; accepted October 2, 1980.
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.