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1 Laboratory of General Biochemistry, University of Chile, Santiago, Chile; Department of Pharmacology, University of Toronto, Toronto, Canada
Chronic administration of ethanol to rats, in a dosage which was previously found to produce acquired behavioral tolerance, resulted in an increase in the rate of K+ and Rb86 accumulation by brain cortex slices incubated in vitro. There was also an increase in (Na + K)-stimulated adenosine triphosphatase activity as measured in brain homogenates. Cessation of alcohol treatment was followed by a return of the rate of cation transport to normal values in about the same time as has previously been observed for the disappearance of acquired tolerance. There was no difference in the inhibitory effect of ethanol added in vitro on the rate of cation transport in brain slices from control and alcohol-treated animals. In the erythrocytes of human alcoholics, Rb86 uptake and membrane (Na + K)-adenosine triphosphatase activity were both increased above normal values. The changes in cation transport and adenosine triphosphatase activity are interpreted as adaptive changes resulting from chronic intake of ethanol.
Submitted on December 23, 1969
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