Abstract
The evidence continues to mount that excessive or prolonged activation of excitatory amino acid (EAA) receptors in the central nervous system contributes to the death of neurones taking place in certain neuropathological conditions of the types that affect humans (Olney 1978; Meldrum and Garthwaite 1990). These conditions include cerebral ischaemia, hypoglycaemia and trauma in which an endogenous agonist, presumably glutamate, is believed to be the culprit. However, following the discoveries that ingestion of the glutamate receptor agonists, domoic acid (in mussels), β-N-oxalylamino-L-alanine (BOAA, in chick peas) and β-N-methyl-amino-L-alanine (BMAA, in the seeds of a false sago palm, Cycas) induces neurodegeneration, attention is also being directed towards glutamate-like chemicals in the environment as neurotoxic agents.
Department of Physiology, University of Liverpool, Brownlow Hill, P.O. Box 147, Liverpool L69 3BX, U.K.
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© 1991 Springer-Verlag Berlin Heidelberg
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Garthwaite, J., Garthwaite, G., Williams, G.D. (1991). Excitatory Amino Acid Neurotoxicity in Rat Brain Slices. In: Ascher, P., Choi, D.W., Christen, Y. (eds) Glutamate, Cell Death and Memory. Research and Perspectives in Neurosciences. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-84526-0_10
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DOI: https://doi.org/10.1007/978-3-642-84526-0_10
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