Abstract
Retigabine is the first approved anticonvulsant that acts via activation of KCNQ2-5 voltage-gated potassium channels, caused by a hyperpolarizing shift in the voltage-dependence of activation. An important unexplored feature of retigabine and its derivatives is their state- and use-dependent properties. Drugs that exhibit use-dependence may have stronger effects with more frequent channel stimulation, enabling selective targeting of hyperexcitable cells. We aimed to generate a detailed understanding of the mechanism of action of various KCNQ channel openers by testing their state- and use-dependent effects on KCNQ2 channels.
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