Hall S M
Division of Anatomy and Cell Biology, UMDS, London.
J Neurocytol. 1993 Jun;22(6):480-90. doi: 10.1007/BF01181567.
The first part of this study is a description of the effect of the intraneural injection of lysophosphatidyl choline into the sciatic nerves of C57BL/Wld mice. This mouse is unusual because its peripheral nerve fibres degenerate very slowly after transection, and few myelomonocytic cells are recruited into the endoneurium after traumatic injury. However, intraneural injection of lysophosphatidyl choline produced a typical demyelinating lesion in which recruited macrophages were active in removal of myelin. In the second part of the study, nerves were transected either before, at the same time as, or some days after, the intraneural injection of lysophosphatidyl choline into the distal stump; the changes within the endoneurium were compared with those seen in distal stumps which had not been injected with lysophosphatidyl choline. Immunohistochemical and ultrastructural examination during the period 1-4 weeks after transection showed that degeneration occurred in the portion of each nerve which had been injected with LPC (and which therefore contained exogenous macrophages) but failed to occur in the portion of nerve which was not penetrated by the injected bolus of lysophosphatidyl choline. It is suggested that the unusual property of sealing off of the tips of the transected axons within the distal stumps may be a significant factor in maintaining 'normal' Schwann cell-axon relationships along transected axons, even though the axons are separated from their cell bodies. Lysophosphatidyl choline destabilises the Schwann cell-axon relationship by initiating myelin breakdown within the Schwann cell. It is suggested that while the Schwann cells remain closely associated with the axons in the distal stumps, they do not behave as denervated cells and consequently may be incapable of signalling their damaged status.
本研究的第一部分描述了向C57BL/Wld小鼠坐骨神经内注射溶血磷脂酰胆碱的效果。这种小鼠不同寻常,因为其外周神经纤维在横断后退化非常缓慢,并且创伤性损伤后很少有骨髓单核细胞被募集到神经内膜。然而,神经内注射溶血磷脂酰胆碱会产生典型的脱髓鞘病变,其中募集的巨噬细胞积极参与髓磷脂的清除。在研究的第二部分中,在向远端残端神经内注射溶血磷脂酰胆碱之前、同时或之后几天进行神经横断;将神经内膜内的变化与未注射溶血磷脂酰胆碱的远端残端的变化进行比较。横断后1 - 4周期间的免疫组织化学和超微结构检查表明,在每条神经中注射了LPC的部分(因此含有外源性巨噬细胞)发生了退化,但在未被注射的溶血磷脂酰胆碱团块穿透的神经部分未发生退化。有人提出,在远端残端内封闭横断轴突末端的这种不寻常特性可能是维持横断轴突沿线“正常”雪旺细胞 - 轴突关系的一个重要因素,即使轴突与其细胞体分离。溶血磷脂酰胆碱通过引发雪旺细胞内的髓磷脂分解来破坏雪旺细胞 - 轴突关系。有人提出,虽然雪旺细胞在远端残端仍与轴突紧密相关,但它们并不表现为去神经细胞,因此可能无法发出其受损状态的信号。