Liver regeneration attenuates increased voluntary alcohol intake evoked by the liver damage.

Liver dysfunction induced in Wistar rats either surgically (by construction of portocaval anastomosis) or chemically (by chronic administration of thioacetamide) led to increased voluntary alcohol intake. Alcohol preference could be attenuated by liver regeneration that was triggered by a two-thirds hepatectomy done on cirrhotic rats. The brain serotonin system was activated in portocaval anastomosis rats and unchanged in thioacetamide-treated rats, thus suggesting that serotonin is not likely to be implicated in the mechanism(s) underlying development of alcohol preference in these rats. Also, tetrahydro-beta-carboline could possibly be excluded from consideration. Neither change in the brain concentration or distribution of tetrahydrobetacarboline after long-term treatment with thioacetamide could be found.

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