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Lewis大鼠急性实验性变应性脑脊髓炎的恢复。神经传导的早期恢复以及施万细胞和少突胶质细胞的修复作用。

Recovery from acute experimental allergic encephalomyelitis in the Lewis rat. Early restoration of nerve conduction and repair by Schwann cells and oligodendrocytes.

作者信息

Pender M P

机构信息

Department of Medicine, University of Queensland, Brisbane, Australia.

出版信息

Brain. 1989 Apr;112 ( Pt 2):393-416. doi: 10.1093/brain/112.2.393.

Abstract

Light and electron microscopic histological studies and electrophysiological studies were performed on Lewis rats with acute experimental allergic encephalomyelitis (EAE) induced by whole spinal cord or myelin basic protein to determine the mechanism of clinical recovery. In these animals, total clinical recovery from complete paraplegia may occur as early as 4 days after the onset of hindlimb weakness. These studies indicate that this recovery occurs at a time when there is restoration of nerve conduction in the peripheral nervous system (PNS) and central nervous system (CNS) and when most demyelinated fibres have been invested, and some partially remyelinated, by Schwann cells or oligodendrocytes in the PNS and CNS, respectively. These findings support the hypothesis that the neurological signs of acute EAE are due to demyelination in the PNS and CNS.

摘要

对由全脊髓或髓鞘碱性蛋白诱导产生急性实验性过敏性脑脊髓炎(EAE)的Lewis大鼠进行了光镜和电镜组织学研究以及电生理研究,以确定临床恢复的机制。在这些动物中,从完全截瘫状态完全临床恢复最早可能在下肢无力发作后4天出现。这些研究表明,这种恢复发生在周围神经系统(PNS)和中枢神经系统(CNS)神经传导恢复之时,且此时PNS和CNS中大多数脱髓鞘纤维已分别被雪旺细胞或少突胶质细胞包裹,部分已重新髓鞘化。这些发现支持了急性EAE的神经学症状是由于PNS和CNS脱髓鞘所致的假说。

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