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实验性糖尿病性神经病变:轴突横截面积改变导致慢速运输受损。

Experimental diabetic neuropathy: impairment of slow transport with changes in axon cross-sectional area.

作者信息

Medori R, Autilio-Gambetti L, Monaco S, Gambetti P

出版信息

Proc Natl Acad Sci U S A. 1985 Nov;82(22):7716-20. doi: 10.1073/pnas.82.22.7716.

DOI:10.1073/pnas.82.22.7716
PMID:2415969
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC391404/
Abstract

Analysis of slow axonal transport in the sciatic and primary visual systems of rats with streptozotocin-induced diabetes of 4-6 weeks duration showed impairment of the transport of neurofilament subunits, tubulin, actin, and a 30- and a 60-kDa polypeptide in both systems. The degree of impairment was not uniform. Transport of polypeptide constituents of the slow component b, such as the 30- and 60-kDa polypeptides, appeared to be more severely affected than the transport of constituents of the slow component a, such as neurofilaments. Morphometric analysis of sciatic axons revealed a proximal increase and a distal decrease of axonal cross-sectional area. It is proposed that impairment of axoplasmic transport and changes of axonal size are related. Transport impairment results in a larger number of neurofilaments, microtubules, and other polypeptides in the proximal region of the axon, which increases in size, whereas fewer neurofilaments, microtubules, and other polypeptides reach the distal axons that show a size decrease. Such changes in axonal transport and area are likely to occur in other diabetic animal models and in human diabetes.

摘要

对链脲佐菌素诱导的病程为4 - 6周的糖尿病大鼠坐骨神经和初级视觉系统中的慢速轴突运输进行分析,结果显示在这两个系统中神经丝亚基、微管蛋白、肌动蛋白以及一种30 kDa和一种60 kDa多肽的运输均受到损害。损害程度并不一致。慢速组分b的多肽成分(如30 kDa和60 kDa多肽)的运输似乎比慢速组分a的成分(如神经丝)的运输受到更严重的影响。对坐骨神经轴突的形态计量学分析显示,轴突横截面积近端增加而远端减小。有人提出轴浆运输受损与轴突大小变化有关。运输受损导致轴突近端区域有更多的神经丝、微管和其他多肽,轴突大小增加,而较少的神经丝、微管和其他多肽到达远端轴突,远端轴突则出现大小减小。轴突运输和面积的这种变化可能在其他糖尿病动物模型以及人类糖尿病中也会发生。

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