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Journal of Neurophysiology, Vol 71, Issue 3 1272-1280, Copyright © 1994 by APS
ARTICLES |
D. J. Surmeier, N. Seno and S. T. Kitai
Department of Anatomy and Neurobiology, College of Medicine, University of Tennessee, Memphis 38163.
1. Large, projection-like neurons from the adult (> 3 wk post-natal) rat globus pallidus (GP) were acutely isolated and subjected to whole-cell voltage-clamp (n = 37). Ca2+ currents were isolated pharmacologically in cells with whole-cell capacitances of 15-34 pF. 2. With 5 mM Ba2+ as a charge carrier, whole-cell currents began to activate near -40 mV and peaked near 0 mV. Based on activation threshold and inactivation kinetics, currents appeared to be of the high-voltage-activated type. 3. Cd2+ blocked whole-cell currents with an IC50 near 2 microM. Currents activated at negative potentials were not relatively resistant to Cd2+, supporting the inference that low-voltage-activated currents were not prominent in these neurons. 4. The dihydropyridine, L-channel antagonist, nifedipine (5 microM), reduced peak current by 21 +/- 4% (SD) (n = 10). The dihydropyridine agonist, BayK 8644 (1-2 microM) enhanced peak current and slowed current deactivation (n = 4). 5. The N-channel antagonist, omega-conotoxin GVIA (omega-CgTx, 2 microM) blocked 25 +/- 7% of the peak whole-cell current (n = 10). The blocks produced by omega-CgTx and nifedipine were additive, blocking an average of 46 +/- 8% of the current (n = 10). 6. The current resistant to the selective N- and L-channel antagonists was partially blocked by the P-channel antagonist omega-agatoxin IVA (omega-AgTx, 100 nM). omega-AgTx blocked about one-half of the current not attributable to N- and L-type channels (22 +/- 5% of the total current, n = 5).(ABSTRACT TRUNCATED AT 250 WORDS)
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