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The Journal of Neuroscience, April 26, 2006, 26(17):4602-4612; doi:10.1523/JNEUROSCI.5204-05.2006

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

Walther Akemann and Thomas Knöpfel

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

Correspondence should be addressed to Dr. Thomas Knöpfel, RIKEN Brain Science Institute, Laboratory for Neuronal Circuit Dynamics, 2-1 Hirosawa, Wako City, Saitama 351-0198, Japan. Email: tknopfel{at}brain.riken.jp

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.

Key words: cerebellum; potassium channels; sodium channel; spike trains; knock-out mice; Purkinje neurons

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Received Dec. 6, 2005; revised March 23, 2006; accepted March 24, 2006.

Correspondence should be addressed to Dr. Thomas Knöpfel, RIKEN Brain Science Institute, Laboratory for Neuronal Circuit Dynamics, 2-1 Hirosawa, Wako City, Saitama 351-0198, Japan. Email: tknopfel{at}brain.riken.jp

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