Nagata H, Brimijoin S, Low P, Schmelzer J D
Department of Pharmacology, Mayo Clinic, Rochester, MN 55905.
Brain Res. 1987 Oct 6;422(2):319-26. doi: 10.1016/0006-8993(87)90939-5.
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.
在经历慢性缺氧的大鼠运动神经中，研究了通过掺入[35S]甲硫氨酸进行放射性标记的蛋白质的慢速轴突运输。实验条件包括将大鼠暴露于含8 - 10%氧气的环境中3周、5周或10周。一个经过实验验证的计算机模型预测，尽管测得循环血红蛋白从16 g%增加到22 g%，但神经内膜平均氧分压仍从30.5 mmHg降至19 mmHg。在缺氧的早期阶段，神经传导速度未受影响。缺氧10周后，坐骨神经的传导速度似乎仍正常，但尾神经的传导速度降低了2.5 - 4.5 m/s。然而，在任何时候都没有证据表明慢速轴突运输受损，其平均运输速度为每天1 - 2 mm。进行了另一组实验，以评估由毒物对溴苯乙酰脲诱导的周围神经病变大鼠运动神经中的慢速轴突运输。结果表明，与仅表现出轻度至中度运动功能障碍的大鼠相比，表现出后肢完全麻痹的大鼠运输速度较低。然而，这种差异可能反映了轻度神经病变中运输的加速。我们认为，在实验性缺氧和毒物诱导的神经病变中的观察结果值得注意，因为慢速运输对神经元环境的扰动具有抗性。
