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

摘要

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 CNS depressant effects of alcohol. Upon alcohol withdrawal however, the increased neural excitability that was adaptive in the presence of alcohol, becomes counteradaptive 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.