Pender M P, Nguyen K B, Willenborg D O
Department of Medicine, University of Queensland, Royal Brisbane Hospital, Australia.
J Neuroimmunol. 1989 Dec;25(2-3):125-42. doi: 10.1016/0165-5728(89)90130-6.
Histological studies were performed on Lewis rats with experimental allergic encephalomyelitis (EAE) passively transferred by myelin basic protein (MBP)-sensitized syngeneic spleen cells in order to determine the relationship between demyelination and neurological signs. Neither inflammation nor demyelination was present on the day prior to the onset of neurological signs but both were present in the spinal roots and spinal cord on the day of onset of tail weakness (4 days after passive transfer). Demyelination and the neurological signs both increased over the next 48 h. There was evidence that the caudal roots were more severely affected than the rostral roots. The peripheral nerves were spared. Demyelination in the spinal cord was concentrated in the dorsal root entry and ventral root exit zones. The initial stages of repair of demyelinated spinal root fibres by Schwann cells were observed on the earliest day that clinical recovery commenced (day 7). At this time some demyelinated fibres were closely associated with debris-free Schwann cells, and occasional fibres were completely invested by 1-2 layers of Schwann cell cytoplasm. Remyelination (compact myelin lamellae formation) by Schwann cells was first observed in the spinal roots on day 9. By the time of complete clinical recovery (day 11) the majority of affected spinal root cores had thin new myelin sheaths. Repair of central nervous system myelin by oligodendrocytes was slower than peripheral nervous system myelin repair. Investment of demyelinated spinal cord axons by oligodendrocytes was observed on day 9, and remyelination by these cells was seen on day 10. We conclude that the neurological signs of passively induced MBP-EAE can be accounted for by demyelination of the lumbar, sacral and coccygeal spinal roots and spinal cord root entry and exit zones, and that the subsequent clinical recovery can be explained by investment and remyelination of demyelinated peripheral and central nervous system fibres by Schwann cells and oligodendrocytes respectively.
为了确定脱髓鞘与神经体征之间的关系，对通过髓鞘碱性蛋白（MBP）致敏的同基因脾细胞被动转移而诱发实验性变态反应性脑脊髓炎（EAE）的Lewis大鼠进行了组织学研究。在神经体征出现前一天，既无炎症也无脱髓鞘现象，但在尾巴无力发作当天（被动转移后4天），脊髓神经根和脊髓中均出现了炎症和脱髓鞘。在接下来的48小时内，脱髓鞘和神经体征均有所增加。有证据表明，尾根比头根受影响更严重。外周神经未受影响。脊髓脱髓鞘集中在背根进入区和腹根穿出区。在临床恢复开始的最早一天（第7天），观察到雪旺细胞对脱髓鞘脊髓神经根纤维的修复初期。此时，一些脱髓鞘纤维与无碎片的雪旺细胞紧密相关，偶尔有纤维被1 - 2层雪旺细胞胞质完全包裹。雪旺细胞的髓鞘再生（紧密髓鞘板层形成）最早在第9天在脊髓神经根中观察到。到完全临床恢复时（第11天），大多数受影响的脊髓神经根核心有薄的新髓鞘。少突胶质细胞对中枢神经系统髓鞘的修复比对周围神经系统髓鞘的修复要慢。少突胶质细胞对脱髓鞘脊髓轴突的包裹在第9天观察到，这些细胞的髓鞘再生在第10天可见。我们得出结论，被动诱导的MBP - EAE的神经体征可由腰骶尾脊髓神经根以及脊髓神经根进出区的脱髓鞘来解释，随后的临床恢复可分别由雪旺细胞和少突胶质细胞对脱髓鞘的周围和中枢神经系统纤维的包裹和髓鞘再生来解释。
