The KCNQ5 Potassium Channel Mediates a Component of the Afterhyperpolarization Current in Mouse Hippocampus
The KCNQ5 potassium channel mediates a component of the afterhyperpolarization current in mouse hippocampus Anastassios V. Tzingounisa,1,2, Matthias Heidenreichb,1, Tatjana Kharkovetsc, Guillermo Spitzmaulb, Henrik S. Jensend,3, Roger A. Nicolla,4, and Thomas J. Jentschb,c,4 aDepartment of Cellular and Molecular Pharmacology and Department of Physiology, University of California, San Francisco, CA 94143; bLeibniz-Institut für Molekulare Pharmakologie (FMP) and Max-Delbrück-Centrum für Molekulare Medizin (MDC), Berlin, D-13125, Germany; cZentrum für Molekulare Neurobiologie (ZMNH), Universität Hamburg, Hamburg, D-20251, Germany; and dDepartment of Medical Physiology, The Panum Institute, University of Copenhagen, Copenhagen, DK-2200, Denmark Contributed by Roger A. Nicoll, April 8, 2010 (sent for review February 18, 2010) Mutations in KCNQ2 and KCNQ3 voltage-gated potassium channels brainstem (18). Unlike KCNQ2 and KCNQ3, the function of lead to neonatal epilepsy as a consequence of their key role in KCNQ5 in the brain remains unknown and no neurological dis- regulating neuronal excitability. Previous studies in the brain have orders have been attributed to it. Given KCNQ5’s similar bio- focused primarily on these KCNQ family members, which contribute physical properties to other members of the KCNQ family, to M-currents and afterhyperpolarization conductances in multiple KCNQ5 may also contribute to M-currents (15, 16). To elucidate brain areas. In contrast, the function of KCNQ5 (Kv7.5), which also the physiological functions of KCNQ5 and test whether KCNQ5 displays widespread expression in the brain, is entirely unknown. also has a role in AHP currents, we generated knock-in (KI) mice Here, we developed mice that carry a dominant negative mutation carrying a dominant negative (dn) mutation in KCNQ5.
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