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Related Experiment Videos

Alcohol intoxication: ion channels and genetics.

R A Harris1, A M Allan

  • 1Denver Veterans Administration Medical Center, Colorado.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
|April 1, 1989
PubMed
Summary

Genetic differences in ion channel function strongly implicate gamma-aminobutyric acid (GABA)-stimulated chloride channels in alcohol intoxication. The roles of calcium and sodium channels in intoxication remain less clear.

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Area of Science:

  • Neuroscience
  • Pharmacology
  • Genetics

Background:

  • Ethanol and anesthetic-gases affect ion channels in brain membranes.
  • Gamma-aminobutyric acid (GABA)-stimulated chloride channels are activated, while voltage-dependent calcium and sodium channels are inhibited.
  • The in vivo relevance of these neurochemical actions for intoxication is debated.

Purpose of the Study:

  • To investigate the in vivo role of specific ion channels in ethanol and benzodiazepine intoxication.
  • To leverage genetic models with varying sensitivities to intoxication.

Main Methods:

  • Utilized animal populations with genetic differences in intoxication sensitivity.
  • Included inbred strains, selected lines, recombinant inbred strains, and heterogeneous stocks.

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  • Examined ion channel function in relation to intoxication phenotypes.

    • Main Results:

    • Genetic variations in ion channel function were analyzed.
    • Strong evidence links GABA-stimulated chloride channel function to intoxication.
    • The contribution of calcium and sodium channels to intoxication is less definitive.

    Conclusions:

    • Genetic studies provide compelling evidence for the involvement of GABA-stimulated chloride channels in ethanol and benzodiazepine intoxication.
    • The precise role of voltage-dependent calcium and sodium channels in intoxication requires further investigation.