Contribution of KCNQ2 and KCNQ3 to the medium and slow afterhyperpolarization currents

摘要: Benign familial neonatal convulsion (BNFC) is a neurological disorder caused by mutations in the potassium channel genes KCNQ2 and KCNQ3, which are thought to contribute medium afterhyperpolarization (mAHP). Despite their importance normal brain function, it unknown whether they invariably function as heteromeric complexes. Here, we examined contribution of KCNQ3 mediating apamin-insensitive mAHP current (ImAHP) hippocampus. The ImAHP was not impaired CA1 pyramidal neurons from mice genetically deficient for either or but reduced ≈50% dentate granule cells. While recording KCNQ-deficient mice, observed that calcium-activated slow (IsAHP) also cells, suggesting KCNQ channels might this whose molecular identity unknown. Further pharmacological experiments manipulating provided evidence support possibility. Together our data suggest multiple subunit compositions can mediate ImAHP, very same subunits may IsAHP. We present neuronal calcium sensor protein hippocalcin allow these dual signaling processes.