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Episodic ataxia type‐1 syndrome (EA‐1) is an autosomal dominant neurological disorder that manifests itself during infancy and results from point mutations in the voltage‐gated potassium channel gene hKv1.1. The hallmark of the disease is continuous myokymia and episodic attacks of spastic contractions of the skeletal muscles, which cause permanent disability. Coexpression of hKv1.1 and hKv1.2 subunits produces heteromeric potassium channels with biophysical and pharmacological properties intermediate between the respective homomers. By using tandemly linked subunits, we demonstrate that hKv1.1 subunits bearing the EA‐1 mutations V408A and E325D combine with hKv1.2 to produce channels with altered kinetics of activation, deactivation, C‐type inactivation, and voltage dependence. Moreover, hKv1.1V408A single‐channel analysis reveals a ∼threefold reduction of the mean open duration of …