Department of Physiology, The School of Medical Sciences, Bristol (U.K.).
Restor Neurol Neurosci. 1991 Jan 1;3(2):65-73. doi: 10.3233/RNN-1991-3203.
Counts of myelinated and unmyelinated axon profiles have been made from normal, uninjured rat sural nerves and from nerves injured 6 months earlier in one of two ways. In one group of rats the nerve was simply cut and left to regenerate, leading to the development of a neuroma in continuity, while in the second group the nerve was cut but then ligated as well to prevent regeneration; this led to stump neuroma formation. After nerve transection and regeneration, with subsequent formation of a neuroma in continuity, there was no change in the number of myelinated axon profiles found 25 mm proximal to the old injury site when compared with control, but there was an 18% reduction (P < 0.05) in the number of unmyelinated axon profiles. Immediately proximal to the injury site the picture was similar, with there still being the same number of myelinated axon profiles as in control material but here the reduction in unmyelinated axon numbers was slightly greater at 24% (P < 0.05). In the proximal part of nerves that had been cut and stump neuroma formation induced there was a large increase (33%) in myelinated axon profiles over and above control values (P < 0.001) but the number of unmyelinated profiles was the same as in controls. Closer to the stump neuroma the number of myelinated axon profiles had increased yet further to be 88% (P < 0.001) above control while the number of unmyelinated ones remained no different from control. Our interpretation of these results is that after nerve transection and regeneration there is no loss of peripheral neurons supporting myelinated axons but some loss of those supporting unmyelinated ones. If a cut nerve is prevented from regenerating and a stump neuroma forms, however, a vigorous sprouting response is triggered in neurons with myelinated axons while those supporting unmyelinated axons are possibly prevented from dying. The reaction of peripheral neurons to injury is such that the number of axons they support varies along the nerve as one goes disto-proximally away from the injury site. Thus discrepancies in results from different laboratories have come about because material for axon counting has been taken from different points along the nerve relative to the injury site and also because the material has been taken from nerves injured in different ways.
已经对正常、未受伤的大鼠腓肠神经以及 6 个月前通过两种方式之一受伤的神经中的髓鞘和无髓鞘轴突进行了计数。在一组大鼠中，神经只是被切断并让其再生，导致连续性神经瘤的形成，而在第二组中，神经被切断但也被结扎以防止再生；这导致残端神经瘤的形成。神经横断和再生后，随着连续性神经瘤的形成，与对照相比，在距离旧损伤部位 25 毫米处发现的有髓鞘轴突的数量没有变化，但无髓鞘轴突的数量减少了 18%（P < 0.05）。在损伤部位的近端，情况类似，与对照材料中一样有相同数量的有髓鞘轴突，但这里无髓鞘轴突数量的减少略大，为 24%（P < 0.05）。在已经被切断并形成残端神经瘤的神经近端，有髓鞘轴突的数量比对照值增加了 33%（P < 0.001），但无髓鞘轴突的数量与对照相同。更靠近残端神经瘤，有髓鞘轴突的数量进一步增加，比对照值高 88%（P < 0.001），而无髓鞘轴突的数量与对照没有区别。我们对这些结果的解释是，在神经横断和再生后，支持有髓鞘轴突的周围神经元没有丢失，但支持无髓鞘轴突的神经元有一些丢失。然而，如果切断的神经不能再生并形成残端神经瘤，则有髓鞘轴突的神经元会触发强烈的发芽反应，而支持无髓鞘轴突的神经元可能会被阻止死亡。周围神经元对损伤的反应是，它们所支持的轴突数量沿着神经从损伤部位向远侧-近侧逐渐变化。因此，不同实验室的结果存在差异，是因为轴突计数的材料是从相对于损伤部位的神经的不同部位获取的，并且还因为材料是从以不同方式受伤的神经中获取的。
