L-beta-N-oxalyl-alpha,beta-diaminopropionic acid toxicity in motor neurons

[摘要]：The excitatory amino acid L-beta-N-oxalyl-alpha,beta-diaminopropionic acid (L-beta-ODAP) in Lathyrus sativus L. is proposed as the causative agent of the neurodegenerative disease neurolathyrism. We investigated the effect of L-beta-ODAP on [Ca2+](i) handling, redox homeostasis, and cell death in rat spinal motor neurons. L-b-ODAP and L-glutamate triggered [Ca2+](i) transients, which were inhibited by the alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptor blockers; 2,3-dioxo-6-nitro-1,2,3, 4-tetrahydrobenzo[f]quinoxaline-7-sulfonamide and 1-naphthyl acetylspermine, the latter specifically blocking Ca2+-permeable alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptors. In addition, 2,3-dioxo-6-nitro1,2,3,4- tetrahydrobenzo[f] quinoxaline-7-sulfonamide, and to a lesser extent 1-naphthyl acetylspermine, protected the neurons against cell death induced by L-beta-ODAP or L-glutamate. Methionine and cysteine were also protective against neuronal cell death. We conclude that deregulation of [Ca2+](i) homeostasis and oxidative stress contribute to motor neuron cell death in neurolathyrism. NeuroReport 22: 131-135 (C) 2011 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins.

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