Medical Journals

Interaction of Kv3 Potassium Channels and Resurgent Sodium Current Influences the Rate of Spontaneous Firing of Purkinje Neurons.

Authors:
  • Akemann Walther
  • Knöpfel Thomas

From: Laboratory for Neuronal Circuit Dynamics, RIKEN Brain Science Institute, Wako City, Saitama 351-0198, Japan.

The Journal of neuroscience : the official journal of the Society for Neuroscience

  • Publish Date: Apr 2006
  • ISSN: 1529-2401
  • Volume: 26
  • Issue: 17
  • Pages: 4602-12
  • Medium: Internet
  • Language: English
  • Citation (JAMA): Akemann Walther, Knöpfel Thomas, et al. Interaction of Kv3 Potassium Channels and Resurgent Sodium Current Influences the Rate of Spontaneous Firing of Purkinje Neurons.. J. Neurosci. Apr 2006;26:4602-12

Abstract

Purkinje neurons spontaneously generate action potentials in the absence of synaptic drive and thereby exert a tonic, yet plastic, input to their target cells in the deep cerebellar nuclei. Purkinje neurons express two ionic currents with biophysical properties that are specialized for high-frequency firing: resurgent sodium currents and potassium currents mediated by Kv3.3. How these ionic currents determine the intrinsic activity of Purkinje neurons has only partially been understood. Purkinje neurons from mutant mice lacking Kv3.3 have a reduced rate of spontaneous firing. Dynamic-clamp recordings demonstrated that normal firing rates are rescued by inserting artificial Kv3 currents into Kv3.3 knock-out Purkinje neurons. Numerical simulations indicated that Kv3.3 increases the spontaneous firing rate via cooperation with resurgent sodium currents. We conclude that the rate of spontaneous action potential firing of Purkinje neurons is controlled by the interaction of Kv3.3 potassium currents and resurgent sodium currents.

Mesh Headings (Keywords): Action Potentials, Animals, Biological Clocks, Cells, Cultured, Ion Channel Gating, Mice, Mice, Inbred C57BL, Mice, Inbred ICR, Mice, Knockout, Potassium, Purkinje Cells, Shaw Potassium Channels, Sodium


Check for Full Text / PubMed Unique Identifier (PMID): 16641240


This abstract is part of PubMed, a service of the U.S. National Library of Medicine. PubMed includes more than 17 million citations from MEDLINE and other life science journals for biomedical articles. See Copyright and Disclaimers.

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The data herein was last updated on July 8th, 2008 and may not reflect the most current and accurate data available from NLM.


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