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Vol. 54, Issue 2, 397-406, August 1998
Department of Pharmacology and Molecular Toxicology (B.C., A.M.D.,
S.N.T.),
Department of Physiology (J.R.L.), and
Interdepartmental
Program in Neuroscience (B.C., A.M.D., J.R.L., S.N.T.), University of
Massachusetts Medical Center, Worcester, Massachusetts 01655
We examined the actions of ethanol on the single channel properties of
large conductance Ca2+-activated K+ (BK)
channels isolated from skeletal muscle T-tubule membranes and
incorporated into planar lipid bilayer membranes. We have taken
advantage of this preparation, because it lacks most elements of
cellular complexity, including cytoplasmic constituents and complex
membrane lipid composition and architecture, to examine the minimum
requirements for the effects of alcohol. Clinically relevant
concentrations (25-200 mM) of ethanol increased the
activity of BK channels incorporated into bilayers composed of
phosphatidylethanolamine (PE) alone or PE and phosphatidylserine. The
potentiation of channel activity by ethanol was attributable
predominantly to a decrease in the average amount of time spent in
closed states. Ethanol did not significantly affect the current
amplitude-voltage relationship for BK channels, indicating that channel
conductance for K+ was unaffected by the drug. Although
base-line characteristics of BK channels incorporated into bilayers
composed only of PE differed from those of channels in PE/
phosphatidylserine in a manner expected from the change in bilayer
charges, the actions of ethanol on channel activity were qualitatively
similar in the different lipid environments. The effects of ethanol on
single channel properties of BK channels in the planar bilayer are very similar to those reported for the action of ethanol on neurohypophysial BK channels studied in native membrane, and for cloned BK channels expressed in Xenopus laevis
oocytes, which suggests that ethanol's site and
mechanism of action are preserved in this greatly simplified preparation.
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