Rydevik B, McLean W G, Sjöstrand J, Lundborg G
J Neurol Neurosurg Psychiatry. 1980 Aug;43(8):690-8. doi: 10.1136/jnnp.43.8.690.
Rapid axonal transport in rabbit vagus nerve was studied during and after graded nerve compression. Proteins of the rapid axonal transport were labelled by micro-injection of 3H-leucine into the nodose ganglion and the cervical vagus nerve was subjected to graded compression by a small "mini-cuff" applied directly to the exposed nerve trunk. The results showed that even slight trauma to the nerve, in this model represented by a pressure at 50 mmHg applied for two hours, may induce accumulation of axonally transported proteins at the level of compression. This transport block was, however, reversible within one day. 200 mmHg and 400 mmHg applied for two hours similarly induced a block of axonal transport persisting up to at least one and three days respectively after the compression. Time for recovery of normal transport was correlated with the magnitude of the pressure applied to the nerve. The results indicate that axons may survive, that is not undergo Wallerian degeneration, after blockage of rapid axonal transport persisting at least one day after the compression trauma.
在分级神经压迫期间及之后,对兔迷走神经的快速轴突运输进行了研究。通过将³H-亮氨酸微量注射到结状神经节中来标记快速轴突运输的蛋白质,并通过直接应用于暴露神经干的小型“微型袖带”对颈迷走神经进行分级压迫。结果表明,在该模型中,即使是对神经的轻微损伤(以50 mmHg的压力施加两小时表示),也可能在压迫部位诱导轴突运输蛋白的积累。然而,这种运输阻滞在一天内是可逆的。施加两小时的200 mmHg和400 mmHg同样诱导了轴突运输阻滞,分别在压迫后至少持续一天和三天。正常运输恢复的时间与施加于神经的压力大小相关。结果表明,在压迫性创伤后,快速轴突运输阻滞持续至少一天后,轴突可能存活,即不会发生华勒变性。