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Am J Physiol Cell Physiol 267: C1452-C1458, 1994;
0363-6143/94 $5.00
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AJP - Cell Physiology, Vol 267, Issue 5 C1452-C1458, Copyright © 1994 by American Physiological Society

ARTICLES

Ketamine inhibition of large conductance Ca(2+)-activated K+ channels is modulated by intracellular Ca2+

D. D. Denson and D. C. Eaton
Department of Anesthesiology, Emory University School of Medicine, Atlanta, Georgia 30322.

The present investigation was conducted to study the relationship between intracellular Ca2+ and inhibition of large conductance Ca(2+)-activated K+ (BK) currents by ketamine using excised patches from GH3 cells. Five ketamine concentrations were studied in the presence of six Ca2+ concentrations. The half-maximal inhibition for BK channel block by ketamine was increased from 4.1 +/- 0.7 microM at 0.1 microM intracellular Ca2+ to 230 +/- 74 microM at 100 microM intracellular Ca2+. Open probability (Po), Ca2+ concentration, and ketamine concentration data were best described by a competitive inhibition model. The inhibition constant for ketamine was 20.5 +/- 5.2 microM, and the Michaelis-Menten constant (Km) value for Ca2+ was 3.58 +/- 0.49 microM, which was not different from Km for Ca2+ in the absence of ketamine (3.33 +/- 0.37 microM). Taken alone, these data would suggest that Ca2+ and ketamine were competing for the same site on the channel protein. However, examination of open and closed interval data from patches containing only one channel show that ketamine primarily produces a decrease in the frequency of long-lived open events, suggesting that the effect of ketamine on BK channels may not be by a direct effect on channel proteins.


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