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RA Harris and P Bruno
Ethanol, diethylether, halothane and enflurane inhibited the veratridine-dependent uptake of 24Na by synaptosomes isolated from rodent brain. The inhibitory action of ethanol was similar for uptake periods of 1 to 10 sec and also was observed with batrachotoxin- stimulated sodium uptake, demonstrating an inhibition of sodium influx through voltage-dependent channels. The inhibitory action of tetrodotoxin on sodium uptake was not altered by ethanol, indicating this site on the sodium channel was not altered by ethanol. The action of ethanol was selective for different brain regions and was more potent in inhibiting sodium uptake in cortex than in cerebellum. Investigation of the effects of temperature on veratridine-stimulated uptake and ethanol actions demonstrated that an increase in temperature (13 degrees-33 degrees C) decreased both the apparent KD of veratridine and the Vmax of the uptake. Ethanol decreased the apparent Vmax at all temperatures and decreased the apparent KD at low 13 degrees and 18 degrees C) but not at higher (30 degrees and 33 degrees C) temperatures. Thus, an increase in temperature mimicked some, but not all, of the effects of ethanol. These results, together with those from other studies, suggest that the disordering of membrane lipids by ethanol and other intoxicant-anesthetic drugs is an important factor in the inhibition of sodium channel function by these drugs.
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