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Related Experiment Videos

Energetic dysfunction in quinolinic acid-lesioned rat striatum

Y M Bordelon1, M F Chesselet, D Nelson

  • 1Department of Pharmacology, University of Pennsylvania, Philadelphia, U.S.A.

Journal of Neurochemistry
|November 5, 1997
PubMed
Summary

Quinolinic acid injection causes progressive mitochondrial dysfunction in rats, impacting energy metabolism. This dysfunction may be key in neurodegenerative diseases like Huntington's disease, offering targets for neuroprotective agents.

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Area of Science:

  • Neuroscience
  • Mitochondrial Biology
  • Cellular Metabolism

Background:

  • Mitochondrial dysfunction is implicated in neurodegenerative diseases, including Huntington's disease.
  • Quinolinic acid, an excitotoxin, induces neuronal death patterns similar to Huntington's disease.
  • The effects of quinolinic acid on striatal energy metabolism are not well understood.

Purpose of the Study:

  • To investigate the time-dependent effects of quinolinic acid on striatal energy metabolism in vivo.
  • To correlate mitochondrial function with nucleotide and amino acid concentrations post-injection.

Main Methods:

  • Intrastriatal injection of quinolinic acid into rat striatum.
  • Quantification of oxygen consumption in free and synaptic mitochondria.

Related Experiment Videos

  • Measurement of nucleotide and amino acid concentrations at various time points.

    • Main Results:

    • A decreased respiratory control ratio in free mitochondria was observed as early as 6 hours post-quinolinic acid injection.
    • By 12 hours, a more pronounced decline in respiratory control ratio (45%) and significant reductions in ATP, NAD, aspartate, and glutamate (30-60%) were noted.
    • No significant changes in nucleotide concentrations were observed at 6 hours.

    Conclusions:

    • In vivo quinolinic acid administration leads to progressive mitochondrial dysfunction.
    • This dysfunction may be a critical event in the cell death cascade of Huntington's disease and related disorders.
    • Assessed indicators of mitochondrial function could aid in evaluating neuroprotective agents.