Watson D F, Griffin J W
J Neuropathol Exp Neurol. 1987 Jan;46(1):96-108. doi: 10.1097/00005072-198701000-00009.
Distal axonal degeneration has been correlated with abnormalities of fast axonal transport in several toxic neuropathies. We have investigated axonal transport in experimental PNU (N-3-pyridylmethyl-N'-p-nitrophenylurea; Vacor) neuropathy, because of the rapid and synchronous degeneration of many terminal axons after a single dose of PNU. Almost all axon terminals at neuromuscular junctions in hindfoot muscles degenerated by 24 hours after the administration of PNU. Fewer affected axons were found in intramuscular nerve twigs, and fewer still in the posterior tibial nerves. No abnormal myelinated axons were found in the sciatic nerve in the thigh. Fast axonal transport in the sciatic nerve remained normal to the mid-thigh, but a reduced amount of labeled transported material reached the posterior tibial nerve at the ankle (27% reduction). Autoradiography showed that nearly no transported material reached the intramuscular nerves and neuromuscular junctions of the hindfeet. These results suggest that toxic impairment of fast anterograde axonal transport may contribute to the axonal degeneration produced by PNU.
在几种中毒性神经病中，远端轴突变性与快速轴突运输异常有关。由于单次给予PNU（N-3-吡啶基甲基-N'-对硝基苯基脲；灭鼠优）后许多终末轴突会迅速且同步地发生变性，我们对实验性PNU神经病中的轴突运输进行了研究。给予PNU后24小时，后足肌肉神经肌肉接头处的几乎所有轴突终末都发生了变性。在肌内神经小分支中发现的受影响轴突较少，在胫后神经中则更少。在大腿的坐骨神经中未发现异常的有髓轴突。坐骨神经中的快速轴突运输在大腿中部之前仍保持正常，但到达踝关节处胫后神经的标记运输物质数量减少（减少了27%）。放射自显影显示，几乎没有运输物质到达后足的肌内神经和神经肌肉接头。这些结果表明，快速顺行性轴突运输的毒性损伤可能导致PNU引起轴突变性。
