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大鼠视网膜顶盖束2,5 -己二醇中毒后的恢复。一项超微结构研究。

Recovery from 2,5-hexanediol intoxication of the retinotectal tract of the rat. An ultrastructural study.

作者信息

Jones H B, Cavanagh J B

出版信息

Acta Neuropathol. 1982;58(4):286-90. doi: 10.1007/BF00688611.

DOI:10.1007/BF00688611
PMID:6891552
Abstract

Rats were given 2,5-hexanediol, a metabolite of n-hexane, in the drinking water until they developed a marked degree of paresis over about 7 weeks and were then allowed to recover naturally. The time course and the manner of removal of the neurofilamentous masses accumulated within axons caused by the intoxication were followed by electron microscopy over the subsequent 8 weeks. The neurofilamentous masses slowly disappeared completely from the axons of this tract, without there being any degeneration, over 6-7 weeks. They disappeared first from the fibres in the brachium of the superior colliculus, perhaps by transport towards the terminals, and later from the axons within the superior colliculus itself. Particularly in preterminal fibres in the superior colliculus the filamentous accumulations became permeated by a network of smooth endoplasmic reticulum which may have played a part in the removal of the filaments. Accumulations of mitochondria and dense bodies in preterminal regions, presumed to be caused by obstruction to retrograde transport, disappeared pari passu with loss of the filaments. The significance of these events in relation to neurofilament metabolism is discussed.

摘要

给大鼠饮用含有正己烷代谢物2,5 -己二醇的水,持续约7周,直至它们出现明显程度的轻瘫,然后让它们自然恢复。在随后的8周内,通过电子显微镜观察中毒引起的轴突内积累的神经丝团块的清除时间进程和方式。在6 - 7周内,这些神经丝团块从该束的轴突中缓慢完全消失,且没有任何退化现象。它们首先从上丘臂的纤维中消失,可能是通过向终末运输,随后从上丘本身的轴突中消失。特别是在上丘的终末前纤维中,丝状聚集体被光滑内质网网络渗透,这可能在细丝的清除中起了作用。终末前区域线粒体和致密体的积累,推测是由逆行运输受阻引起的,随着细丝的消失而同步消失。讨论了这些事件与神经丝代谢的关系。

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本文引用的文献

1
Electron microscopy of experimental degeneration in the avian optic tectum.鸟类视顶盖实验性退变的电子显微镜观察
J Anat. 1962 Jul;96(Pt 3):309-316.5.
2
The relationship of glucose utilization and morphological change in the visual system in hexacarbon neuropathy.六碳化合物神经病中视觉系统葡萄糖利用与形态学变化的关系。
Brain Res. 1981 Oct 19;222(2):447-51. doi: 10.1016/0006-8993(81)91053-2.
3
On the pattern of changes in the rat nervous system produced by 2,5 hexanediol. A topographical study by light microscopy.关于2,5 -己二醇对大鼠神经系统产生的变化模式。光镜下的局部解剖学研究。
在光照或黑暗条件下暴露于2,5 -己二醇对白化和有色大鼠视网膜的影响。II. 电生理学
Arch Toxicol. 1993;67(6):435-41. doi: 10.1007/BF01977406.
Brain. 1981 Jun;104(2):297-318. doi: 10.1093/brain/104.2.297.
4
The pattern of recovery of axons in the nervous system of rats following 2,5-hexanediol intoxication: a question of rheology?2,5-己二醇中毒后大鼠神经系统轴突的恢复模式:流变学问题?
Neuropathol Appl Neurobiol. 1982 Jan-Feb;8(1):19-34. doi: 10.1111/j.1365-2990.1982.tb00254.x.
5
Properties of a calcium-activated protease in squid axoplasm which selectively degrades neurofilament proteins.鱿鱼轴质中一种选择性降解神经丝蛋白的钙激活蛋白酶的特性。
J Neurobiol. 1980;11(1):1-12. doi: 10.1002/neu.480110102.
6
The early evolution of neurofilamentous accumulations due to 2,5-hexanediol in the optic pathways of the rat.大鼠视路中2,5 -己二醇所致神经丝聚集的早期演变
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7
n-hexane polyneuropathy. An occupational disease of shoemakers.正己烷多发性神经病。一种鞋匠的职业病。
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8
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9
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10
Environmental hydrocarbons produce degeneration in cat hypothalamus and optic tract.环境碳氢化合物会导致猫的下丘脑和视束发生退化。
Science. 1978 Jan 13;199(4325):199-200. doi: 10.1126/science.413192.