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Related Experiment Videos

Endogenous excitotoxic agents.

T W Stone, J H Connick, P Winn

    Ciba Foundation Symposium
    |January 1, 1987
    PubMed
    Summary
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    Quinolinic acid is a potential endogenous neurotoxin that activates N-methyl-aspartate receptors, leading to cell death. Its effects are counteracted by kynurenic acid, suggesting a balance regulates central nervous system excitability.

    Area of Science:

    • Neuroscience
    • Neurochemistry

    Background:

    • Glutamate and aspartate are potential neurotransmitters but require high concentrations for adult toxicity due to efficient uptake.
    • Endogenous neurotoxins are implicated in central nervous system (CNS) cell death.

    Purpose of the Study:

    • To identify endogenous neurotoxins and understand their mechanisms of action.
    • To investigate the role of quinolinic acid and kynurenic acid in neurotoxicity and CNS excitability.

    Main Methods:

    • The study discusses the neurotoxic effects of quinolinic acid and its interaction with N-methyl-aspartate (NMDA) receptors.
    • It examines the antagonistic role of kynurenic acid on quinolinic acid's neurotoxic actions.

    Main Results:

    • Quinolinic acid induces cell death by activating NMDA receptors.

    Related Experiment Videos

  • Differences in quinolinate and N-methyl-aspartate activity suggest NMDA receptor subpopulations.
  • Kynurenic acid antagonizes the excitatory and neurotoxic effects of quinolinic acid.

    • Conclusions:

    • Quinolinic acid is a strong candidate for an endogenous neurotoxin.
    • A balance between quinolinic acid and kynurenic acid concentrations may regulate CNS excitability and cell death.