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Anticonvulsant effects of the BK‐channel antagonist paxilline

Purpose:  Mutations that enhance currents through the Ca2+‐ and voltage‐gated K+ channel BK (Slo, maxiK, KCNMA1) have been associated with seizure disorders in both rodent models and humans. Previously we have found that seizures themselves induce a gain‐of‐function in BK channels that is associated with elevated excitability in neocortical neurons. In this study, we sought to examine whether administration of BK‐channel antagonists possess anticonvulsant activity in vivo.