Brodie C, Sampson S R
Department of Life Sciences, Bar-Ilan University, Ramat-Gan, Israel.
J Pharmacol Exp Ther. 1987 Sep;242(3):1098-103.
Ethanol was studied for its effects on electrophysiological properties of cultured skeletal myotubes prepared from fetal or neonatal rats. Intracellular recordings were made with KCl-filled (3 M) glass micropipettes from cells 7 to 9 days after plating. Ethanol produced a temperature-dependent, dose-related depolarization of the myotubes. Maximum depolarization of 15 mV was reached at a concentration of 217 mM at 37 degrees C; at 25 degrees C, ethanol caused hyperpolarization at low concentration (21.7 mM) and was without effect at higher concentrations (up to 435 mM). Of other alcohols examined, only propanol had a significant effect on transmembrane resting potential (Em). In the presence of ouabain, a specific Na-K pump inhibitor, ethanol had no effect on Em. Ethanol decreased the relation between Em and [K+]o. At 37 degrees C, spontaneously occurring action potentials were abolished completely by ethanol, but at 25 degrees C their frequency was reduced. Amplitude, overshoot, rates of rise and fall were all increased by ethanol (21.7 mM). We also found that ouabain-dependent 86Rb uptake was decreased by 217 mM ethanol at 37 degrees C and was without effect at 25 degrees C, and that this phenomenon was increased by 21.7 mM ethanol at the lower temperature. We conclude that ethanol effects on Em are exerted primarily via changes in activity and contribution of the Na-K pump to Em.
