title: Effects of β-ODAP and its biosynthetic precursor on the electrophysiological activity of cloned glutamate receptors.
abstract: 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.
authors.affiliation: Laboratory of Biology, Nihon University College of Pharmacy, Funabashi, Chiba 274, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Kusama-Eguchi
authors.forename: F
authors.initials: F
authors.lastname: Ikegami
authors.forename: T
authors.initials: T
authors.lastname: Kusama
authors.forename: F
authors.initials: F
authors.lastname: Lambein
authors.forename: K
authors.initials: K
authors.lastname: Watanabe