K. Kusamaeguchi et al., EFFECTS OF BETA-ODAP AND ITS BIOSYNTHETIC PRECURSOR ON THE ELECTROPHYSIOLOGICAL ACTIVITY OF CLONED GLUTAMATE RECEPTORS, Environmental toxicology and pharmacology, 2(4), 1996, pp. 339-342
3-N-Oxalyl-L-2,3-diaminopropanoic acid (beta-ODAP) induces neurolathyr
ism, a motor neuron disease. To elucidate the pathogenic mechanism of
this process, the action of beta-ODAP on the excitatory amino acid (EA
A) receptor-mediated currents was examined using cloned EAA receptors
expressed in Xenopus oocytes. On the voltage-clamp recordings of an AM
PA receptor(alpha(1)/alpha(2) heterooligomer), beta-ODAP was a strong
agonist on this receptor, the potency being almost the same as L-gluta
mate. On the other hand, beta-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. beta-
ODAP may cause the neurodegenerative disease, neurolathyrism, mainly t
hrough the excitotoxic interaction with AMPA receptors.