Effects of Thiamin Deprivation and Antagonism on Voluntary Ethanol Intake in Rats

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Abstract
The role of acetaldehyde, brain dopamine and noradrenaline in the regulation of voluntary ethanol intake by thiamin-deficient rats was studied. Thiamin deficiency was produced by dietary deprivation of thiamin (TD) or by subcutaneous daily injections of one of the thiamin antagonists, pyrithiamin (PT, 500 µg/kg body weight) and oxythiamin (OT, 2,000 µg/kg). Treatment for 10 days with PT, a thiamin analog known to cause rapid depletion of brain thiamin, increased voluntary consumption of 10% (v/v) ethanol by 180% from intial consumption levels. In PT-treated rats, blood acetaldehyde concentrations induced by intraperitoneal injection of 1.5 g ethanol/kg body weight were three times higher than in the controls. TD increased ethanol intake by about 100% but blood acetaldehyde concentrations were not affected. Treatment with OT, a thiamin analog which does not enter the brain, did not affect ethanol intake but slightly increased blood acetaldehyde concentrations. OT-treated rats showed anorexia from the beginning of treatment, while in PT-treated rats anorexia did not appear until the days 10–14 combined with motor dysfunction and decreased ethanol intake. No differences in the concentrations of dopamine or noradrenaline in the whole-brain homogenate were found. The results suggest that blood acetaldehyde is not involved in the control of voluntary ethanol consumption in thiamin-deficient rats, and neither is increased ethanol intake a result of reduction in food intake induced by thiamin deficiency. Increased ethanol drinking in rats by thiamin deficiency seems to be related to the roles of thiamin in brain.