Moss T H
J Neurol Sci. 1981 Feb;49(2):207-22. doi: 10.1016/0022-510x(81)90079-4.
Schwann cell function in the dystonic mutant mouse was studied by grafting peripheral nerve from normal into affected littermates of a C57/BL (Fa.) dt dystonic mouse colony and vice versa. In a control experiment, only unaffected animals of the colony were used, and nerve isografts were found to be ultrastructurally indistinguishable from normal nerve autografts. In addition, the isografts showed no features of the lymphocytic inflammatory rejection reaction observed in normal nerve allografts, and there was evidence that donor Schwann cells remained viable and were active in all isografts examined. When nerve isografts from affected dystonic mutants were implanted into normal littermate nerves, the normal host axons regenerating through the grafted region acquired degenerative changes characteristic of naturally occurring dystonic peripheral nerve. These changes were not seen in the host axons regenerating either outside the dystonic graft regions, or more distally in the host nerve stumps. When normal nerve isografts were implanted into affected dystonic mutant nerves, the dystonic axons regenerated through the normal graft region and became normally myelinated. It is concluded that an underlying Schwann cell defect may be responsible for the abnormalities of the dystonic mouse peripheral neuropathy.
通过将正常的外周神经移植到C57/BL（Fa.）dt肌张力障碍小鼠群体的患病同窝仔鼠中，反之亦然，研究了肌张力障碍突变小鼠中雪旺细胞的功能。在对照实验中，仅使用该群体中未受影响的动物，发现神经同基因移植在超微结构上与正常神经自体移植无法区分。此外，同基因移植未表现出正常神经异体移植中观察到的淋巴细胞炎性排斥反应特征，并且有证据表明供体雪旺细胞在所有检查的同基因移植中保持存活并活跃。当将来自受影响的肌张力障碍突变体的神经同基因移植植入正常同窝仔鼠神经中时，通过移植区域再生的正常宿主轴突获得了自然发生的肌张力障碍外周神经特有的退行性变化。在肌张力障碍移植区域外再生的宿主轴突或宿主神经残端更远端再生的宿主轴突中未见到这些变化。当将正常神经同基因移植植入受影响的肌张力障碍突变体神经中时，肌张力障碍轴突通过正常移植区域再生并正常髓鞘化。得出的结论是，潜在的雪旺细胞缺陷可能是肌张力障碍小鼠外周神经病变异常的原因。
