Volume 868, Issue 1 p. 304-343

Contributions of Kv3 Channels to Neuronal Excitability

BERNARDO RUDY

Corresponding Author

BERNARDO RUDY

Department of Physiology and Neuroscience, and Department of Biochemistry, New York University of Medicine, New York, New York 10016, USA

Address for correspondence: Department of Physiology and Neuroscience, New York University School of Medicine, 550 First Avenue, New York 10016. e-mail: [email protected]Search for more papers by this author
ALAN CHOW

ALAN CHOW

Department of Physiology and Neuroscience, and Department of Biochemistry, New York University of Medicine, New York, New York 10016, USA

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DAVID LAU

DAVID LAU

Department of Physiology and Neuroscience, and Department of Biochemistry, New York University of Medicine, New York, New York 10016, USA

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YIMY AMARILLO

YIMY AMARILLO

Department of Physiology and Neuroscience, and Department of Biochemistry, New York University of Medicine, New York, New York 10016, USA

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ANDER OZAITA

ANDER OZAITA

Department of Physiology and Neuroscience, and Department of Biochemistry, New York University of Medicine, New York, New York 10016, USA

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MICHAEL SAGANICH

MICHAEL SAGANICH

Department of Physiology and Neuroscience, and Department of Biochemistry, New York University of Medicine, New York, New York 10016, USA

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HERMAN MORENO

HERMAN MORENO

Department of Physiology and Neuroscience, and Department of Biochemistry, New York University of Medicine, New York, New York 10016, USA

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MARCELA S. NADAL

MARCELA S. NADAL

Department of Physiology and Neuroscience, and Department of Biochemistry, New York University of Medicine, New York, New York 10016, USA

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RICARDO HERNANDEZ-PINEDA

RICARDO HERNANDEZ-PINEDA

Department of Physiology and Neuroscience, and Department of Biochemistry, New York University of Medicine, New York, New York 10016, USA

Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, México.

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ARTURO HERNANDEZ-CRUZ

ARTURO HERNANDEZ-CRUZ

Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, México.

Department of Physiology and Neuroscience, and Department of Biochemistry, New York University of Medicine, New York, New York 10016, USA

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ALEV ERISIR

ALEV ERISIR

Department of Physiology, New York Medical College, Valhalla, New York, USA

Department of Physiology and Neuroscience, and Department of Biochemistry, New York University of Medicine, New York, New York 10016, USA

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CHRISTOPHER LEONARD

CHRISTOPHER LEONARD

Department of Physiology, New York Medical College, Valhalla, New York, USA

Department of Physiology and Neuroscience, and Department of Biochemistry, New York University of Medicine, New York, New York 10016, USA

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ELEAZAR VEGA-SAENZ DE Miera

ELEAZAR VEGA-SAENZ DE Miera

Department of Physiology and Neuroscience, and Department of Biochemistry, New York University of Medicine, New York, New York 10016, USA

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First published: 06 February 2006
Citations: 252

Abstract

ABSTRACT: Four mammalian Kv3 genes have been identified, each of which generates, by alternative splicing, multiple protein products differing in their C-terminal sequence. Products of the Kv3.1 and Kv3.2 genes express similar delayed-rectifier type currents in heterologous expression systems, while Kv3.3 and Kv3.4 proteins express A-type currents. All Kv3 currents activate relatively fast at voltages more positive than −10 mV, and deactivate very fast. The distribution of Kv3 mRNAs in the rodent CNS was studied by in situ hybridization, and the localization of Kv3.1 and Kv3.2 proteins has been studied by immunohistochemistry. Most Kv3.2 mRNAs (∼90%) are present in thalamic-relay neurons throughout the dorsal thalamus. The protein is expressed mainly in the axons and terminals of these neurons. Kv3.2 channels are thought to be important for thalamocortical signal transmission. Kv3.1 and Kv3.2 proteins are coexpressed in some neuronal populations such as in fast-spiking interneurons of the cortex and hippocampus, and neurons in the globus pallidus. Coprecipitation studies suggest that in these cells the two types of protein form heteromeric channels. Kv3 proteins appear to mediate, in native neurons, similar currents to those seen in heterologous expression systems. The activation voltage and fast deactivation rates are believed to allow these channels to help repolarize action potentials fast without affecting the threshold for action potential generation. The fast deactivating current generates a quickly recovering afterhyperpolarization, thus maximizing the rate of recovery of Na+ channel inactivation without contributing to an increase in the duration of the refractory period. These properties are believed to contribute to the ability of neurons to fire at high frequencies and to help regulate the fidelity of synaptic transmission. Experimental evidence has now become available showing that Kv3.1-Kv3.2 channels play critical roles in the generation of fast-spiking properties in cortical GABAergic interneurons.