Environ Toxicol Pharmacol 1996 Dec 20;24:339-42. doi: 10.1016/s1382-6689(96)00067-1.

Effects of β-ODAP and its biosynthetic precursor on the electrophysiological activity of cloned glutamate receptors.

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3-N-Oxalyl-l-2,3-diaminopropanoic acid (β-ODAP) induces neurolathyrism, a motor neuron disease. To elucidate the pathogenic mechanism of this process, the action of β-ODAP on the excitatory amino acid (EAA) receptor-mediated currents was examined using cloned EAA receptors expressed in Xenopus oocytes. On the voltage-clamp recordings of an AMPA receptor (α (1)α (2) heterooligomer), β-ODAP was a strong agonist on this receptor, the potency being almost the same as l-glutamate. On the other hand, β-ODAP had little effect on the glutamate-evoked currents through the expressed NMDA receptor (NR1(A)/NR2A), but showed a weak inhibitory effect on the glycine-modulatory site. β-ODAP may cause the neurodegenerative disease, neurolathyrism, mainly through the excitotoxic interaction with AMPA receptors.

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