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Effect of β-N-oxalyl-L-α, β-diaminopropionic acid on glutamate uptake by synaptosomes

Abstract

THE unusual amino acid β-N-oxalyl-L-α, β-diaminopropionic acid (ODAP), isolated from the seeds of Lathyrus sativus is a potent neurotoxin1–3. It produces biochemical changes in the brain typical of an excitant amino acid and is implicated in the aetiology of human neurolathyrism caused by eating the seeds of L. sativus4–6. It may act as a glutamate antagonist: ODAP inhibits glutamate oxidation7 possibly by inhibiting glutamate uptake in bovine brain mitochondria; it also acts as a competitive inhibitor of glutamate uptake in certain strains of yeast8, and a similar process might occur at the synaptic level. Any effect of ODAP on glutamate uptake at synapses is significant in view of the neurotransmitter function of glutamate, which seems to be neuroexcitory as well as neurotoxic9–12. But Balcar and Johnston13 have shown with rat brain slices that ODAP does not inhibit the glutamate uptake by the high affinity system.

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LAKSHMANAN, J., PADMANABAN, G. Effect of β-N-oxalyl-L-α, β-diaminopropionic acid on glutamate uptake by synaptosomes. Nature 249, 469–471 (1974). https://doi.org/10.1038/249469a0

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