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The Journal of Neuroscience, May 21, 2008, 28(21):5570-5581; doi:10.1523/JNEUROSCI.0747-08.2008

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Cellular/Molecular
Ablation of Kv3.1 and Kv3.3 Potassium Channels Disrupts Thalamocortical Oscillations In Vitro and In Vivo

Felipe Espinosa,¹ Miguel A. Torres-Vega,¹ Gerald A. Marks,² and Rolf H. Joho¹

Departments of ¹Neuroscience and ²Psychiatry, The University of Texas Southwestern Medical Center at Dallas, Dallas, Texas 75390-9111

Correspondence should be addressed to Dr. Rolf Joho, Department of Neuroscience, University of Texas Southwestern Medical Center at Dallas, 5323 Harry Hines Boulevard, Dallas, TX 75390-9111. Email: rolf.joho{at}utsouthwestern.edu

The genes Kcnc1 and Kcnc3 encode the subunits for the fast-activating/fast-deactivating, voltage-gated potassium channels Kv3.1 and Kv3.3, which are expressed in several brain regions known to be involved in the regulation of the sleep–wake cycle. When these genes are genetically eliminated, Kv3.1/Kv3.3-deficient mice display severe sleep loss as a result of unstable slow-wave sleep. Within the thalamocortical circuitry, Kv3.1 and Kv3.3 subunits are highly expressed in the thalamic reticular nucleus (TRN), which is thought to act as a pacemaker at sleep onset and to be involved in slow oscillatory activity (spindle waves) during slow-wave sleep. We showed that in cortical electroencephalographic recordings of freely moving Kv3.1/Kv3.3-deficient mice, spectral power is reduced up to 70% at frequencies <15 Hz. In addition, the number of sleep spindles in vivo as well as rhythmic rebound firing of TRN neurons in vitro is diminished in mutant mice. Kv3.1/Kv3.3-deficient TRN neurons studied in vitro show 60% increase in action potential duration and a reduction in high-frequency firing after depolarizing current injections and during rebound burst firing. The results support the hypothesis that altered electrophysiological properties of TRN neurons contribute to the reduced EEG power at slow frequencies in the thalamocortical network of Kv3-deficient mice.

Key words: parvalbumin; fast-spiking interneurons; thalamic reticular nucleus; spindle waves; rhythmic rebound bursts; cortical activation

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Received Feb. 18, 2008; revised April 18, 2008; accepted April 21, 2008.

Correspondence should be addressed to Dr. Rolf Joho, Department of Neuroscience, University of Texas Southwestern Medical Center at Dallas, 5323 Harry Hines Boulevard, Dallas, TX 75390-9111. Email: rolf.joho{at}utsouthwestern.edu

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