Key result
Genetic deficiency of KCNQ2 or KCNQ3 reduced the apamin-insensitive mAHP current and calcium-activated slow afterhyperpolarization current by approximately 50% in dentate granule cells of mice.
Multiple KCNQ subunit compositions can mediate the ImAHP, and these same subunits may also contribute to the IsAHP, potentially facilitated by hippocalcin.
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Mouse findings on KCNQ2/3 in mAHP/IsAHP leave open human neuronal roles; prospective studies needed before any clinical consideration.
Tzingounis et al. (2008) studied Benign familial neonatal convulsion (BNFC). Genetic deficiency of KCNQ3 or KCNQ2 vs. Wild-type mice was evaluated on apamin-insensitive mAHP current (ImAHP) and calcium-activated slow afterhyperpolarization current (IsAHP). Genetic deficiency of KCNQ2 or KCNQ3 reduced the apamin-insensitive mAHP current and calcium-activated slow afterhyperpolarization current by approximately 50% in dentate granule cells of mice.
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