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Related Experiment Videos

L-cysteine, a bicarbonate-sensitive endogenous excitotoxin.

J W Olney1, C Zorumski, M T Price

  • 1Washington University School of Medicine, Department of Psychiatry, St. Louis, MO 63110.

Science (New York, N.Y.)
|May 4, 1990
PubMed
Summary

L-cysteine causes neurotoxicity by activating glutamate receptors, especially N-methyl-D-aspartate receptors. Its excitotoxic effects are amplified by bicarbonate, suggesting a role in neurodegenerative diseases.

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Area of Science:

  • Neuroscience
  • Neurochemistry

Background:

  • L-cysteine is a naturally occurring amino acid found in the brain and environment.
  • The neurotoxic mechanisms of L-cysteine have remained unclear.
  • Previous research has implicated other excitotoxins in neurodegenerative disorders.

Purpose of the Study:

  • To elucidate the underlying mechanism of L-cysteine-induced neurotoxicity.
  • To investigate the role of glutamate receptors in L-cysteine neurotoxicity.
  • To determine the influence of bicarbonate on L-cysteine's excitotoxic potential.

Main Methods:

  • Systemic administration of L-cysteine to immature rodents.
  • In vitro and in vivo neurotoxicity assays.
  • Assessment of receptor involvement (NMDA and quisqualate receptors).

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  • Evaluation of bicarbonate ion concentration effects.

    • Main Results:

    • L-cysteine causes neuronal destruction in the cerebral cortex, hippocampus, thalamus, and striatum.
    • Neurotoxicity is primarily mediated by N-methyl-D-aspartate (NMDA) receptors.
    • Quisqualate receptors contribute to toxicity at higher L-cysteine concentrations.
    • Bicarbonate significantly potentiates the excitotoxic potency of L-cysteine.

    Conclusions:

    • L-cysteine acts as a potent excitotoxin, primarily through NMDA receptor activation.
    • Bicarbonate significantly enhances L-cysteine's neurotoxic effects.
    • The findings suggest a potential role for L-cysteine in central nervous system neurodegenerative processes.