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• W1988209218 abstract "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. Methods: Seizures were induced in animals by intraperitoneal (i.p.) injection of the γ-aminobutyric acid (GABA)A antagonists picrotoxin or pentylenetetrazole. Twenty-four hours following induction of the initial seizure episode, animals were reinjected with chemoconvulsant in the presence of the BK-channel antagonist paxilline or saline. The presence and duration of tonic–clonic seizures were evaluated. Results: Intraperitoneal injection of paxilline was sufficient to eliminate tonic–clonic seizures in picrotoxin-treated animals. Paxilline reduced seizure duration and intensity in pentylenetetrazole-injected animals. Discussion: The BK-channel antagonist paxilline possesses significant anticonvulsant activity in both picrotoxin and pentylenetetrazole seizure models, an effect that may be related to the seizure-dependent gain-of-function in BK channel previously observed in neocortical neurons in vitro." @default.
• W1988209218 created "2016-06-24" @default.
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• W1988209218 date "2009-04-01" @default.
• W1988209218 modified "2023-10-14" @default.
• W1988209218 title "Anticonvulsant effects of the BK-channel antagonist paxilline" @default.
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• W1988209218 doi "https://doi.org/10.1111/j.1528-1167.2008.01888.x" @default.
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