Thiamine deficiency neuropathy in rats : K. Kunze and E. Muskat (Giessen, Germany)

Abstract

Thiamine deficiency has been implicated as a signifccant contributing factor in the development of peripheral neuropathies in chronic alcoholic patients. We hypothezized that thiamine deficiency may lead to an alteration in axonal transport because it has been associated with “dying-back” neuropathies and its importance in neural tissue has been demonstrated with antimetabolites. To test this possibility rats were made thiamine-deficient by feeding a liquid diet lacking thiamine. Control rats were pair-fed a complete liquid diet. The deficiency developed after 3 to 4 weeks and was evidenced by anorexia, weight-loss, and a significant increase in the erythrocyte transketolase activity ratio. Also, the sural nerve conduction velocity was found to be significantly reduced in these animals (18.74 m/s) relative to that of pair-fed control rats (31.99 m/s). In vitro transport experiments utilizing dorsal root ganglia-sciatic nerve preparations indicated that twice as much [35S]methionine-labeled protein accumulated at a ligation by fast transport in the thiamine-deficient rats as in nerves of their pair-fed controls. There was no difference in the level of incorporation of radioactive precursor into the dorsal root ganglia. The increase in transport suggests that thiamine deficiency per se has no detrimental effects on the transport machinery and process, but may indicate extensive regenerative activity in the distal portions of these axons.