Abstract

Some 200 amino acids have been isolated from plants, but only about 10% of these are normal constituents of mammalian nervous tissue. Many of the other 90% structurally resemble certain of those present in nervous tissue, such that they may compete with the corresponding “normal” amino acid at one or more of its receptor sites, with consequent adverse effects on the nervous system. These receptor sites for amino acids may be on enzymes, transport carriers, or synaptic membranes. With the increasing acceptance of the concept of particular amino acids, especially γ-aminobutyric acid (GABA), glycine, and glutamic and aspartic acids, functioning as major synaptic transmitters in the mammalian central nervous system (Curtis and Johnston, 1974), it appears likely that the neurotoxicity of certain plant amino acids results from interference with amino acid-mediated synaptic transmission. The “antimetabolite” properties of toxic amino acids, particularly in microorganisms, have been extensively studied and have been reviewed by Fowden et al. (1967); this chapter is concerned with some amino acids of plant and fungal origin that adversely influence the mammalian central nervous system after systemic administration.

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