BK通道基因表达会导致对乙醇戒断性癫痫发作的易感性。
Susceptibility to ethanol withdrawal seizures is produced by BK channel gene expression.
作者信息
Ghezzi Alfredo, Krishnan Harish R, Atkinson Nigel S
机构信息
Section of Neurobiology and Waggoner Center for Alcohol and Addiction Research, The University of Texas at Austin, Austin, TX, USA.
出版信息
Addict Biol. 2014 May;19(3):332-7. doi: 10.1111/j.1369-1600.2012.00465.x. Epub 2012 Jun 27.
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 Ca(2+) -activated K(+) channel gene slo in the production of alcohol withdrawal seizures.
摘要
酒精戒断性癫痫发作是严重酒精依赖症状学的一部分，据信其源于长期的神经适应性变化，这些变化可对抗酒精对中枢神经系统的抑制作用。然而，在酒精戒断时，在酒精存在下具有适应性的神经兴奋性增加变得具有反适应性，并产生失衡的过度活跃的神经系统。对于一些个体而言，戒酒揭示出这种失衡就足以引发癫痫发作。利用果蝇模式生物，我们证明了BK型钙激活钾通道基因slo在酒精戒断性癫痫发作产生过程中起核心作用。
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