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Science 19 August 1988:
Vol. 241. no. 4868, pp. 973 - 975
DOI: 10.1126/science.3136549
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Articles

Science, Vol 241, Issue 4868, 973-975
Copyright © 1988 by American Association for the Advancement of Science

articles

Beta-N-methylamino-L-alanine neurotoxicity: requirement for bicarbonate as a cofactor

JH Weiss and DW Choi

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.


THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES:
METABOLISM AND PHARMACOKINETICS OF A DIPEPTIDYL PEPTIDASE IV INHIBITOR IN RATS, DOGS, AND MONKEYS WITH SELECTIVE CARBAMOYL GLUCURONIDATION OF THE PRIMARY AMINE IN DOGS.
M. G. Beconi, A. Mao, D. Q. Liu, C. Kochansky, T. Pereira, C. Raab, P. Pearson, and S.-H. Lee Chiu (2003)
Drug Metab. Dispos. 31, 1269-1277
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Glutamate as a Neurotransmitter in the Brain: Review of Physiology and Pathology.
B. S. Meldrum (2000)
J. Nutr. 130, 1007
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Guam ALS-PDC: possible causes.
P. Spencer, G. Kisby, S. Ross, D. Roy, J Hugon, A. Ludolph, and P. Nunn (1993)
Science 262, 825-826
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L-cysteine, a bicarbonate-sensitive endogenous excitotoxin.
J. Olney, C Zorumski, M. Price, and J Labruyere (1990)
Science 248, 596-599
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