Decreased axonal transport in rat nerve following acute and chronic ethanol exposure.
The axonal transport system, which supplies essential proteins and other cellular components to the distal portions of peripheral nerve axons, has been postulated to be the primary site of vulnerability inducing the peripheral neuropathies associated with neurotoxin exposure. Axonal transport was examined in normal rat dorsal root ganglia-sciatic nerve preparations incubated 28 hours in vitro in the presence of 79, 198 or 395 mg% ethanol. Exposure of the nerves to 395 mg% ethanol significantly reduced the accumulation of radiolabeled protein by 70%. Also, groups of rats were pair-fed an ethanol or isocaloric control diet for 9, 16 or 28 weeks. In vitro axonal transport was found to be unchanged in nerves of rats fed the ethanol diet for 9 weeks, but was significantly reduced 44% after 16 weeks and 47% after 28 weeks of ethanol feeding. These results suggest that interference with the axonal transport machinery by ethanol or perhaps acetaldehyde, its primary metabolite, may lead to the development of alcoholic peripheral neuropathy.
D000437:Alcoholism / Q000473:pathology; D000818:Animals; D001370:Axonal Transport / Q000187:drug effects*; D004305:Dose-Response Relationship, Drug; D000431:Ethanol / Q000494:pharmacology*; D006801:Humans; D008297:Male; D008870:Microtubules / Q000187:drug effects; D051381:Rats; D011919:Rats, Inbred Strains; D012584:Sciatic Nerve / Q000187:drug effects
D000431:Ethanol