Delayed rectifier currents in rat globus pallidus neurons are attributableto Kv2.1 and Kv3.1/3.2 K+ channels

The symptoms of Parkinson disease are thought to result in part from increa sed burst activity in globus pallidus neurons. To gain a better understandi ng of the factors governing this activity, we studied delayed rectifier Kconductances in acutely isolated rat globus pallidus (GP) neurons, using wh ole-cell voltage-clamp and single-cell RT-PCR techniques. From a holding po tential of -40 mV, depolarizing voltage steps in identified GP neurons evok ed slowly inactivating K+ currents. Analysis of the tail currents revealed rapidly and slowly deactivating currents of similar amplitude, The fast com ponent of the current deactivated with a time constant of 11.1 +/- 0.8 msec at -40 mV and was blacked by micromolar concentrations of 4-AP and TEA (K- D similar to 140 mu M). 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 similar to 6 mM). Organic antagonists of Kv1 fa mily channels had little or no effect on somatic currents. These properties are consistent with the hypothesis that the rapidly deactivating current i s 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 b alance of these two channel types could underlie the emergence of burst fir ing after dopamine-depleting lesions.