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Susceptibility to ethanol withdrawal seizures is produced by BK channel gene expression

Authors

  • Alfredo Ghezzi,

    1. Section of Neurobiology and Waggoner Center for Alcohol and Addiction Research, The University of Texas at Austin, Austin, TX, USA
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  • Harish R. Krishnan,

    1. Section of Neurobiology and Waggoner Center for Alcohol and Addiction Research, The University of Texas at Austin, Austin, TX, USA
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  • Nigel S. Atkinson

    Corresponding author
    1. Section of Neurobiology and Waggoner Center for Alcohol and Addiction Research, The University of Texas at Austin, Austin, TX, USA
    • Correspondence to: Nigel Atkinson, The University of Texas at Austin, Section of Neurobiology, 1 University Station, C0920, Austin, TX 78712-0248, USA. E-mail: NigelA@mail.utexas.edu

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Abstract

Alcohol withdrawal seizures are part of the symptomatology of severe alcohol dependence and are believed to originate from long-term neural adaptations that counter the central nervous system depressant effects of alcohol. Upon alcohol withdrawal, however, the increased neural excitability that was adaptive in the presence of alcohol becomes counter-adaptive and produces an imbalanced hyperactive nervous system. For some individuals, the uncovering of this imbalance by alcohol abstention can be sufficient to generate a seizure. Using the Drosophila model organism, we demonstrate a central role for the BK-type Ca2+-activated K+ channel gene slo in the production of alcohol withdrawal seizures.

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