The slow axonal transport of
proteins radiolabeled by incorporation of [35S]
methionine was studied in motor nerves of rats subjected to chronic
hypoxia. The conditions involved exposure to an atmosphere of 8-10%
oxygen for periods of 3, 5, or 10 weeks. An experimentally verified computer model predicted a drop in mean endoneurial
oxygen tension from 30.5 to 19 mm Hg, despite a measured increase in circulating
hemoglobin from 16 to 22 g%. Nerve conduction velocity was unaffected during the early stages of
hypoxia. After 10 weeks of
hypoxia, conduction velocity still appeared normal in the sciatic nerve but was reduced in the caudal nerve by 2.5-4.5 m/s. At no time, however, was there evidence of impaired slow axonal transport, which proceeded with a mean velocity between 1 and 2 mm/day. Another set of experiments was performed to evaluate slow axonal transport in motor nerves of rats with
peripheral neuropathy induced by the toxicant,
p-bromophenylacetylurea. The results suggested a lower transport velocity in rats showing total hind-limb
paralysis as compared with rats showing only mild to moderate motor dysfunction. The difference, however, could have reflected accelerated transport in mild neuropathy. In our view, the observations in experimental
hypoxia- and toxicant-induced neuropathy are noteworthy for the resistance of slow transport to perturbation of the neuronal environment.