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ArticlesCopyright © 1988 by American Association for the Advancement of Science
Beta-N-methylamino-L-alanine neurotoxicity: requirement for bicarbonate as a cofactor
Department of Neurology, Stanford University Medical Center, Stanford 94305.
Ingestion of the excitotoxic cycad seed amino acid beta-N-methylamino-L-alanine may be responsible for the neuronal degeneration associated with Guam amyotrophic lateral sclerosis-parkinsonism-dementia in man. However, the basis for the central neurotoxicity of beta-N-methylamino-L-alanine has been unclear, as it lacks the omega acidic (or equivalent electronegative) moiety characteristic of other excitatory amino acids. beta-N-methylamino-L-alanine produced neurotoxic and neuroexcitatory effects in murine cortical cell cultures only when physiological concentrations of bicarbonate were available in the extracellular bathing medium. Bicarbonate may interact noncovalently with beta-N-methylamino-L-alanine to produce, in combination, a molecular configuration that activates glutamate receptors.
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Science. ISSN 0036-8075 (print), 1095-9203 (online)
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