Interactions between Schwann cell and axon during reinnervation to the motor endplate

采用免疫荧光组织化学方法，观察坐骨神经挤压伤后1~8周轴突、雪旺细胞与细胞外物质在运动终板再支配过程中相互作用的增龄性变化。用激光共聚焦扫描显微镜进行观察。为了确定再生神经纤维的结构成分的分布和共定位，用一些特异性抗体标记轴突(神经细丝，PGP9.5)、雪旺细胞(S 100)、黏附分子[神经细胞黏附分子]。(n-CAM)]和细胞外物质(Tenascin)。此外，还研究了再生神经与乙酰胆碱受体(AChR)之间的结构联系。在老年动物中，神经再支配过程中的主要异常包括偶见的前终末和终末轴突，它们要么走扭曲的路线，要么受损。最明显的变化是终末雪旺细胞变性一致。在运动终板中，神经或遗弃的AChR在再神经支配过程中尤其晚被发现。雪旺细胞周围N-CAM样免疫反应的分布和连续性错乱，再生轴突通过的Tenascin通路构建不完整。综上所述，这些结果表明轴突引导的障碍与突触的不完全重塑相结合，突触接触的有效面积减少。这可能是由于神经再生过程中雪旺细胞、轴突和细胞外物质与年龄相关的不同步成熟所致。

Age-related changes of the interactions between the axon, Schwann cell and extracellular material on reinnervation to the motor endplate were examined during the period of I-8 weeks after crush injury of the sciatic nerve with immunonuofluorescence histochemistry. Observations were done by confocal laser scanning microscopy. To define the distribution and co-localization of the structural components of the regenerating nerve fibers, some specific antibodies were used to label axons (neurofilament, PGP 9.5), Schwann cells (S 100), adhesion molecules [neural cell adhesion molecule. (N-CAM)] and the extracellular material (tenascin). In addition, the structural associations between regenerating nerves and acetylcholine receptors (AChR) were also examined. In the aged animal, the main abnormalities in the process of reinnervation consisted of occasional preterminal and terminal axons which either took a distorted course or were damaged. The most obvious changes was the consistency with degeneration of the terminal Schwann cells. In the motor endplate, loci of aneural or abandoned AChR were frequently found particularly late in the reinnervation process. The distribution and continuities of N-CAM-like immunoreactivity around the Schwann cells Were deranged, and the tenascin pathway through which regenerating axons pass was incompletely constructed. These results taken together indicate disturbance in the axonal guidance coupled with incomplete reformation of synapses with a decrease in the effective area of synaptic contact. This may be due to an age-related unsynchronous maturation among the Schwann cells, axon, and extracellular material during the nerve regeneration.