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Objective: Ion channels belonging to subfamily A of voltage-gated potassium channels (K1) are highly expressed on axons, where they play a key role in determining resting membrane potential, in shaping action potentials, and in modulating action potential frequency during repetitive neuronal firing. We aimed to study the genesis of seizures caused by mutations affecting K1 channels and searched for potential therapeutic targets.

Methods: We used a novel in silico model, the laminar cortex model (LCM), to examine changes in neuronal excitability and network dynamics associated with loss-of-function mutations in K1 channels.

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