Abstract
An experimental model of chronic alcoholic neuropathy in the rat was produced by schedule-induced polydipsia. A mild distal axonal neuropathy in the ventral caudal nerve was found after 16 weeks exposure to about 12g of absolute alcohol per Kg body weight per day. The rats appeared not to be deficient in thiamine, suggesting that the axonal degeneration was due to the direct toxic effect of alcohol. Axonal transport studies indicated a significant increase in the amount of acetylcholinesterase transported in an orthograde direction in the sciatic nerves of alcoholic rats.