Abstract
Abstract— δ‐Aminolaevulinic acid (δ‐ALA) is an omega amino acid structurally similar to γ‐aminobutyric acid (GABA) and l‐glutamate. We have examined the effect of δ‐ALA on the uptake and efflux of radiolabelled GABA and l‐glutamate in rat cortical synaptosomes and report: (1) low concentrations of δ‐ALA reduced the potassium‐stimulated release of [3H]GABA from the synaptosome preparation. This effect was reversed by the GABA receptor antagonist bicuculline. We postulate that GABA release is modulated by a feedback mechanism on presynaptic GABA receptors, and that δ‐ALA has agonist activity at these receptors. (2) δ‐ALA at high concentrations (0.75‐5.0 mm) stimulated the efflux of l‐[14C]glutamate from preloaded synaptosomes. (3) δ‐ALA had no effect on potassium‐stimulated release of l‐glutamate. (4) Uptake of labelled l‐glutamate was inhibited by δ‐ALA in a noncompetitive fashion. (5) Synaptosomes did not accumulate [14C]δ‐ALA in the range 0.5‐50 δm. These results are discussed in relation to the control of GABA release from nerve endings, and the role of δ‐ALA in the neuropsychiatric manifestations of the acute porphyric attack.
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