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糖尿病BB/W大鼠的视觉诱发电位受损及视神经原发性轴索性病变

Impaired visual evoked potential and primary axonopathy of the optic nerve in the diabetic BB/W-rat.

作者信息

Sima A A, Zhang W X, Cherian P V, Chakrabarti S

机构信息

Department of Pathology, University of Michigan, Ann Arbor.

出版信息

Diabetologia. 1992 Jul;35(7):602-7. doi: 10.1007/BF00400249.

DOI:10.1007/BF00400249
PMID:1644237
Abstract

The spontaneously diabetic BB/W-rat has emerged as an important model system for somatic and autonomic diabetic polyneuropathy. In this study we examined visual evoked potentials and the presence of morphometric and structural changes in the optic nerve and the retinal ganglion cells and their afferent axons contained in the retinal nerve fibre layer. A six-month duration of diabetes mellitus was associated with significant increases in the latencies of the visual evoked potentials. The latency of the first positive potential showed a 44% increase, and that of the first negative potential was prolonged by 41%. No significant changes were demonstrated at any of the amplitudes. In the optic nerve mean myelinated fibre size was significantly reduced to 82% of control values, which was accounted for by a significant reduction in axonal size. Axo-glial dysjunction, a prominent structural defect of diabetic somato-sensory neuropathy in both man and diabetic rodents, was non-significantly increased in the optic nerve. In diabetic animals retinal ganglion cells displayed dystrophic changes. No such changes were observed in age- and sex-matched control animals. Proximal axons of the retinal nerve fibre layer showed an increase in dystrophic axons in diabetic BB/W-rats. Morphometric analysis of optic nerve capillaries revealed no abnormalities except for basement membrane thickening. The present data suggest that the diabetic BB/W-rat develops a central sensory neuropathy, characterized functionally by prolonged latencies of the visual evoked potentials and structurally by an axonopathy of optic nerve fibres.

摘要

自发性糖尿病BB/W大鼠已成为研究躯体和自主神经糖尿病性多发性神经病变的重要模型系统。在本研究中,我们检测了视觉诱发电位,以及视神经、视网膜神经节细胞及其包含在视网膜神经纤维层中的传入轴突的形态计量学和结构变化。糖尿病病程6个月与视觉诱发电位潜伏期显著延长有关。第一个正电位的潜伏期增加了44%,第一个负电位的潜伏期延长了41%。各波幅均未显示出显著变化。视神经中平均有髓纤维大小显著减小至对照值的82%,这是由轴突大小显著减小所致。轴突-神经胶质分离是人类和糖尿病啮齿动物糖尿病躯体感觉神经病变的一个突出结构缺陷,在视神经中虽有增加但无统计学意义。糖尿病动物的视网膜神经节细胞出现营养不良性改变。在年龄和性别匹配的对照动物中未观察到此类变化。糖尿病BB/W大鼠视网膜神经纤维层的近端轴突中营养不良性轴突增多。对视神经毛细血管的形态计量学分析显示,除基底膜增厚外无异常。目前的数据表明,糖尿病BB/W大鼠发生了中枢感觉神经病变,其功能特征为视觉诱发电位潜伏期延长,结构特征为视神经纤维轴突病。

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Methylglyoxal Disrupts Paranodal Axoglial Junctions via Calpain Activation.甲基乙二醛通过钙蛋白酶激活破坏连接神经节段的轴突-胶质连接。
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