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The Journal of Neuroscience, August 1, 1999, 19(15):6394-6404

Delayed Rectifier Currents in Rat Globus Pallidus Neurons Are Attributable to Kv2.1 and Kv3.1/3.2 K⁺ Channels

Gytis Baranauskas, Tatiana Tkatch, and D. James Surmeier

Department of Physiology/Northwestern University Institute for Neuroscience, Northwestern University Medical School, Chicago, Illinois 60611

The symptoms of Parkinson disease are thought to result in part from increased burst activity in globus pallidus neurons. To gain a better understanding of the factors governing this activity, we studied delayed rectifier K⁺ conductances in acutely isolated rat globus pallidus (GP) neurons, using whole-cell voltage-clamp and single-cell RT-PCR techniques. From a holding potential of 40 mV, depolarizing voltage steps in identified GP neurons evoked slowly inactivating K⁺ currents. Analysis of the tail currents revealed rapidly and slowly deactivating currents of similar amplitude. The fast component of the current deactivated with a time constant of 11.1 ± 0.8 msec at 40 mV and was blocked by micromolar concentrations of 4-AP and TEA (K_D ~140 µM). The slow component of the current deactivated with a time constant of 89 ± 10 msec at 40 mV and was less sensitive to TEA (K_D = 0.8 mM) and 4-AP (K_D ~6 mM). Organic antagonists of Kv1 family channels had little or no effect on somatic currents. These properties are consistent with the hypothesis that the rapidly deactivating current is attributable to Kv3.1/3.2 channels and the slowly deactivating current to Kv2.1-containing channels. Semiquantitative single-cell RT-PCR analysis of Kv3 and Kv2 family mRNAs supported this conclusion. An alteration in the balance of these two channel types could underlie the emergence of burst firing after dopamine-depleting lesions.

Key words: globus pallidus; delayed rectifier; Kv2.1; Kv3.1/3.2; voltage clamp; single-cell RT-PCR; TEA; 4-AP; potassium channels

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Copyright © 1999 Society for Neuroscience  0270-6474/99/19156394-11$05.00/0

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