EFFECT OF DELTA-AMINOLEVULINIC-ACID ON THE UPTAKE AND EFFLUX OF [H-3]GABA IN RAT-BRAIN SYNAPTOSOMES

§‐Aminolaevulinic acid (§‐ALA) is an omega amino acid which can be considered as an analogue of γ‐aminobutyric acid (GABA). We have examined the effect of §‐ALA on [3H]GABA uptake and release in the synaptosome fraction of rat cerebral cortex and report: (1) High concentrations of §‐ALA (0.75‐5 mM) stimulated [3H]GABA release very markedly, the stimulation with 1mM and 5mM‐§‐ALA exceeding the maximum obtainable with unlabelled GABA; (2) Low concentrations of §‐ALA (0.1‐0.5 mM) produced little stimulation of [3H]GABA efflux, less than that produced by similar concentrations of unlabelled GABA; (3) 0.1 mM‐§‐ALA reduced the stimulation of [3H]GABA efflux elicited by 55 mM‐K+ and the combination of 1 mM‐§‐ALA and 55mM‐K+ produced a lower stimulation of efflux than 1 mM‐§‐ALA alone; (4) §‐ALA inhibits [3H]GABA uptake in a linearly competitive fashion and inhibition is maximal at 0.5 mM‐§‐ALA. These results are discussed in relation to the neuronal high affinity GABA transport mechanism and inhibition of the synaptosomal Na+ and K+ ‐dependent ATPase. It is also postulated that §‐ALA increases the chloride conductance of the synaptosomal membrane, possibly by acting on presynaptic GABA receptors. Copyright © 1979, Wiley Blackwell. All rights reserved