Electroconvulsive seizure thresholds and kindling acquisition rates are altered in mouse models of human KCNQ2 and KCNQ3 mutations for benign familial neonatal convulsions

Purpose:  Benign familial neonatal convulsions (BFNC) is caused by mutations in the KCNQ2 and KCNQ3 genes, which encode subunits of the M‐type potassium channel. The purpose of this study was to examine the effects of orthologous BFNC‐causing mutations on seizure thresholds and the acquisition of corneal kindling in mice with heterozygous expression of the mutations.

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