The Effect of Delta‐aminolaevulinic Acid on the Uptake and Efflux of [³h]gaba in Rat Brain Synaptosomes

Abstract §‐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 [ 3 H]GABA uptake and release in the synaptosome fraction of rat cerebral cortex and report: (1) High concentrations of §‐ALA (0.75‐5 mM) stimulated [ 3 H]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 [ 3 H]GABA efflux, less than that produced by similar concentrations of unlabelled GABA; (3) 0.1 mM‐§‐ALA reduced the stimulation of [ 3 H]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 [ 3 H]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.