Animal models of alcoholic neuropathy: morphologic, electrophysiologic, and biochemical findings.
A chronic high alcohol intake was induced in rats through the use of two procedures: the schedule-induced polydipsia technique and the liquid diet technique. Rats consumed 11-12 g of ethanol per kilogram body weight per day for 16 to 18 weeks. Morphologic evidence of a mild distal axonal neuropathy in the ventral caudal nerve was proposed. The red blood cell transketolase levels were normal, indicating that the rats were not deficient in thiamine and suggesting that the axonal degeneration was due to the direct toxic effect of alcohol. Axonal transport studies demonstrated a significant increase in the amount of acetylcholinesterase transported in an orthograde direction in the sciatic nerves of alcohol-exposed rats, and indicated no change in the transport of choline acetyltransferase or in the specific binding of colchicine by neurotubulin.
D000110:Acetylcholinesterase / Q000378:metabolism; D000437:Alcoholism / Q000150:complications* / Q000473:pathology / Q000503:physiopathology; D000818:Animals; D001369:Axons / Q000201:enzymology; D004032:Diet; D004195:Disease Models, Animal; D004594:Electrophysiology; D000431:Ethanol / Q000008:administration & dosage; D006801:Humans; D008297:Male; D008854:Microscopy, Electron; D010525:Peripheral Nerves / Q000473:pathology / Q000648:ultrastructure; D010523:Peripheral Nervous System Diseases / Q000139:chemically induced* / Q000503:physiopathology; D051381:Rats
D000431:Ethanol; D000110:Acetylcholinesterase