Beta- N -Methylamino-L-Alanine Neurotoxicity: Requirement for Bicarbonate as a Cofactor
- 19 August 1988
- journal article
- Published by American Association for the Advancement of Science (AAAS) in Science
- Vol. 241 (4868), 973-975
- https://doi.org/10.1126/science.3136549
Abstract
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.Keywords
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