Popović M, Bresjanac M, Sketelj J
Institute of Pathology, School of Medicine, University of Ljubljana, Slovenia.
J Neuropathol Exp Neurol. 1994 Nov;53(6):590-7. doi: 10.1097/00005072-199411000-00006.
The role of regenerating axons in the restructuring of the endoneurium into minifascicles after peripheral nerve injury was investigated. Endoneurial changes were studied in the control distal stumps of crushed rat sciatic nerves and in the distal nerve stumps in which, in addition to other cellular elements, the original perineurium had also been destroyed by freezing and thawing. Injured nerves in which axonal regeneration had been prevented were examined for comparison. The changes were observed at light microscopic and ultrastructural levels. Two weeks after nerve injury, incipient endoneurial restructuring by proliferating endoneurial fibroblast-like cells was observed in the distal nerve stumps in all groups of animals. By 4 weeks, the endoneurial changes in control regenerating nerves (crush only) displayed no progress. On the contrary, extensive minifascicular reorganization of the endoneurium was observed in the distal nerve stumps in which the original perineurial barrier had been eliminated. The cells that encircled the minifascicles in the nerves with regenerating axons looked like differentiated perineurial cells, whereas in the absence of regenerating axons, the endoneurial cells that encircled the neurilemmal tubes mostly lacked typical features of the perineurial cells. Therefore, persistent perineurial damage is necessary to induce complete endoneurial compartmentalization. In this case, the regenerating axons enhance differentiation of the endoneurial fibroblast-like cells into the perineurial cells.
研究了再生轴突在周围神经损伤后神经内膜重构为微束中的作用。在大鼠坐骨神经挤压伤对照远端残端以及远端神经残端中研究神经内膜变化，在后一种情况中，除其他细胞成分外，原始的神经束膜也已通过冻融破坏。检查了阻止轴突再生的损伤神经作为对照。在光镜和超微结构水平观察变化。神经损伤两周后，在所有动物组的远端神经残端中均观察到神经内膜成纤维样细胞增殖引起的早期神经内膜重构。到4周时，对照再生神经（仅挤压伤）中的神经内膜变化没有进展。相反，在原始神经束膜屏障已消除的远端神经残端中观察到神经内膜广泛的微束重组。在有再生轴突的神经中围绕微束的细胞看起来像分化的神经束膜细胞，而在没有再生轴突的情况下，围绕神经膜管的神经内膜细胞大多缺乏神经束膜细胞的典型特征。因此，持续的神经束膜损伤是诱导完整神经内膜分隔所必需的。在这种情况下，再生轴突增强神经内膜成纤维样细胞向神经束膜细胞的分化。
