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营养不良小鼠腓总神经中轴突与施万细胞的非典型关系:一项超微结构研究。

Atypical axon-Schwann cell relationships in the common peroneal nerve of the dystrophic mouse: an ultrastructural study.

作者信息

Jaros E, Bradley W G

出版信息

Neuropathol Appl Neurobiol. 1979 Mar-Apr;5(2):133-47. doi: 10.1111/j.1365-2990.1979.tb00666.x.

Abstract

Several atypical features of myelination of the peripheral nervous system are reported in common peroneal nerve of dystrophic mice (129 Re J dy/dy): (i) central nervous system-like contact between myelin sheaths of adjacent nerve fibres; (ii) nodes and internodes of myelinated fibres enwrapped with cytoplasmic processes of Schwann cells from adjacent nerve fibres; (iii) Schwann cells of adjacent nerve fibres co-operating in formation of a single myelin sheath; and (iv) a single Schwann cell myelinating two separate axons. In view of the presence of similar features of myelination in the central nervous system, where the myelin producing cells lack basement membrane, we suggest that in the dystrophic peripheral nerves the development of these features can be attributed to the partial deficiency of the Schwann cell basement membrane. Two types of widened nodes of Ranvier are also identified: (i) nodes with paranodal damage; and (ii) nodes without paranodal damage. In addition, abnormal features of myelination are described which are likely to represent altered Schwann cell/axon relationships during demyelination and remyelination and/or decreased myelinating ability of Schwann cells. We interpret these findings as indicating a metabolic disorder of Schwann cells. They provide an experimental model for the investigation of factors involved in the origin and maintenance of the structural organization of peripheral nerve.

摘要

在营养不良小鼠(129 Re J dy/dy)的腓总神经中,报道了周围神经系统髓鞘形成的几个非典型特征:(i)相邻神经纤维的髓鞘之间存在类似中枢神经系统的接触;(ii)有髓纤维的结和结间被相邻神经纤维的施万细胞的胞质突起包裹;(iii)相邻神经纤维的施万细胞协同形成单个髓鞘;(iv)单个施万细胞为两条独立的轴突形成髓鞘。鉴于中枢神经系统中存在类似的髓鞘形成特征,其中产生髓鞘的细胞缺乏基底膜,我们认为在营养不良的周围神经中,这些特征的出现可归因于施万细胞基底膜的部分缺陷。还识别出两种类型的朗飞结增宽:(i)伴有结旁损伤的结;(ii)无结旁损伤的结。此外,还描述了髓鞘形成的异常特征,这些特征可能代表脱髓鞘和再髓鞘化过程中施万细胞/轴突关系的改变和/或施万细胞髓鞘形成能力的下降。我们将这些发现解释为表明施万细胞存在代谢紊乱。它们为研究参与周围神经结构组织起源和维持的因素提供了一个实验模型。

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