Abstract
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.
Original language | English (US) |
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Pages (from-to) | 6394-6404 |
Number of pages | 11 |
Journal | Journal of Neuroscience |
Volume | 19 |
Issue number | 15 |
DOIs | |
State | Published - Aug 1 1999 |
Keywords
- 4-AP
- Delayed rectifier
- Globus pallidus
- Kv2.1
- Kv3.1/3.2
- Potassium channels
- Single- cell RT-PCR
- TEA
- Voltage clamp
ASJC Scopus subject areas
- General Neuroscience