Endogenous excitotoxic agents.

T. W. Stone, J. H. Connick, P. Winn, M. H. Hastings, M. English

Research output: Chapter in Book/Report/Conference proceedingChapter

40 Citations (Scopus)

Abstract

Although glutamate and aspartate are among the most likely compounds to function as central neurotransmitters, and both can produce cell death in neonatal animals, the efficient uptake systems for these amino acids mean that exceptionally high concentrations are required for toxicity in adults. A better candidate for an endogenous neurotoxin is quinolinic acid, which produces cell death via activation of the N-methyl-aspartate receptors. Several differences of detail between the activity of quinolinate and N-methyl-aspartate may indicate the existence of subpopulations of the N-methyl-aspartate receptor. Another compound in the same 'kynurenine' pathway as quinolinate, kynurenic acid, is an antagonist of the excitatory and neurotoxic actions of quinolinate, and the overall excitability of the central nervous system and the occurrence of cell death may therefore result from a balance between the concentrations of quinolinate and kynurenate.
Original languageEnglish
Title of host publicationCiba Foundation Symposium 126 ‐ Selective Neuronal Death
Chapter13
Pages204-220
Number of pages17
Volume126
DOIs
Publication statusPublished - 1 Jan 1987

Publication series

NameCiba Foundation Symposium
PublisherWiley Subscription Services
ISSN (Print)0300-5208

Keywords

  • aspartic acid
  • glutamic acid
  • glutamic acid derivative
  • quinolinic acid
  • quinolinic acid derivative
  • biological model
  • cell survival
  • central nervous system
  • cytology
  • dementia
  • epilepsy
  • nerve cell

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  • Cite this

    Stone, T. W., Connick, J. H., Winn, P., Hastings, M. H., & English, M. (1987). Endogenous excitotoxic agents. In Ciba Foundation Symposium 126 ‐ Selective Neuronal Death (Vol. 126, pp. 204-220). (Ciba Foundation Symposium). https://doi.org/10.1002/9780470513422.ch13