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

Research Laboratories of the State Alcohol Monopoly (Alko), Box 350, SF-00101 Helsinki 10, Finland

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.

KEY WORDS: • thiamin deficiency • pyrithiamin • oxythiamin • voluntary ethanol drinking • blood acetaldehyde • noradrenaline • dopamine

¹ Present address: School of Medicine, Department of Pharmacology, University of North Carolina, Chapel Hill, NC 27514. However, send reprint requests to: Dr. Hertta-Maija Häkkinen, Alko, Box 350, SF-00101 Helsinki 10, Finland.

Manuscript received 19 July 1979.