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蛋白质缺乏的幼鼠外周神经纤维变性。一项超微结构研究。

Peripheral nerve fibre degeneration in protein-deprived young rats. An ultrastructural study.

作者信息

Oldfors A, Persson M

出版信息

Acta Neuropathol. 1982;57(1):1-6. doi: 10.1007/BF00688871.

Abstract

In a previous study the occurrence of nerve fibre degeneration with a distribution as in dying-back neuropathies was described in young rats subjected to severe protein deprivation (Oldfors 1981). In this study the ultrastructural appearance of the degeneration of the nerve fibres at different levels of the longitudinal tail nerve in severely protein-deprived rats has been investigated. Various structural changes were noted, the most common being bands of Bŭngner indistinguishable from those seen in Wallerian degeneration. In nerve fibres which were less severely affected the most common finding was shrinkage of the axon with concomitant folding of the myelin sheath. Other structural changes included axonal accumulation of 10 nm filaments or mitochondria and other cell organelles, areas of demyelination, and projections of axolemma and Schwann cell membrane into the axon. Signs of axonal regeneration occurred but were infrequent. The degenerative changes seen at various levels of the nerves support the view that the neuropathy is of distal axonal type, but the structural appearance differs from several of the toxic dying-back neuropathies.

摘要

在先前的一项研究中,已描述了在遭受严重蛋白质缺乏的幼鼠中出现了神经纤维变性,其分布如同逆行性神经病(Oldfors,1981)。在本研究中,已对严重蛋白质缺乏大鼠的纵向尾神经不同水平处神经纤维变性的超微结构外观进行了研究。观察到了各种结构变化,最常见的是与华勒氏变性中所见的那些难以区分的Büngner带。在受影响较轻的神经纤维中,最常见的发现是轴突收缩并伴有髓鞘折叠。其他结构变化包括10纳米细丝、线粒体及其他细胞器在轴突中的积聚、脱髓鞘区域以及轴膜和施万细胞膜向轴突内的突出。出现了轴突再生的迹象,但并不常见。在神经的不同水平处所见的退行性变化支持了这种神经病是远端轴突型的观点,但结构外观与几种中毒性逆行性神经病不同。

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