Retrograde axonal transport in chronic ethanol-fed and thiamine-deficient rats

Retrograde axonal transport may play an important role in the feedback regulation of protein synthesis in neuronal perikarya, and the anterograde axonal transport of protein. The "dying-back" neuropathies associated with thiamine deficiency and chronic alcoholism may arise as a consequence of altered axonal transport. We have reported alterations in fast anterograde axonal transport in rats as a result of ethanol exposure or thiamine deficiency. The present studies were undertaken to determine whether retrograde transport was also affected by these experimental treatments. One group of rats was fed a liquid diet containing 6.7% ethanol for 16 weeks. Another group of rats was made thiamine deficient with a thiamine-free diet for 4 weeks. Retrograde axonal transport was labeled by injecting the left sciatic nerve unilaterally with 3H-N-succinimidyl propionate. This compound covalently labels proteins in the nerve at the site of injection and is accumulated by retrograde axonal transport to sensory nerve cell bodies in the dorsal root ganglia and motor nerve cell bodies in the spinal cord. After 7 days, dorsal root ganglia of chronic ethanol-fed rats showed a significant 45% decrease in the amount of accumulated retrograde label compared to controls. No significant differences in accumulation were found in the spinal cords. These results suggest that the peripheral neuropathies caused by chronic alcoholism and thiamine deficiency follow different etiologies, and that motor and sensory fibers are affected differently by ethanol.