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The Journal of Neuroscience, September 3, 2003, 23(22):8077-8091
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MinK-Related Peptide 2 Modulates Kv2.1 and Kv3.1 Potassium Channels in Mammalian Brain
Zoe A. McCrossan,1 Anthony Lewis,1 Gianina Panaghie,1,3 Peter N. Jordan,1,4 David J. Christini,1 Daniel J. Lerner,1,2 andGeoffrey W. Abbott1,2 1Division of Cardiology, Department of Medicine, 2Department of Pharmacology, 3Graduate Program in Pharmacology, and 4Graduate Program in Physiology and Biophysics, Weill Medical College of Cornell University, New York, New York 10021
Delayed rectifier potassium current diversity and regulation are essential for signal processing and integration in neuronal circuits. Here, we investigated a neuronal role for MinK-related peptides (MiRPs), membrane-spanning modulatory subunits that generate phenotypic diversity in cardiac potassium channels. Native coimmunoprecipitation from rat brain membranes identified two novel potassium channel complexes, MiRP2-Kv2.1 and MiRP2-Kv3.1b. MiRP2 reduces the current density of both channels, slows Kv3.1b activation, and slows both activation and deactivation of Kv2.1. Altering native MiRP2 expression levels by RNAi gene silencing or cDNA transfection toggles the magnitude and kinetics of endogenous delayed rectifier currents in PC12 cells and hippocampal neurons. Computer simulations predict that the slower gating of Kv3.1b in complexes with MiRP2 will broaden action potentials and lower sustainable firing frequency. Thus, MiRP2, unlike other known neuronal
subunits, provides a mechanism for influence over multiple delayed rectifier potassium currents in mammalian CNS via modulation of
subunits from structurally and kinetically distinct subfamilies.
Key words: delayed rectifier; hippocampus; KCNE3; Kv2.1; Kv3.1; potassium channel; RNAi
Received June 9, 2003; revised July 5, 2003; accepted July 10, 2003.
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