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金鱼视神经纤维再生过程中的胶质增生:一项免疫组织化学研究。

Gliosis during optic fiber regeneration in the goldfish: an immunohistochemical study.

作者信息

Levine R L

机构信息

Department of Biology, McGill University, Montréal, Quebec, Canada.

出版信息

J Comp Neurol. 1991 Oct 22;312(4):549-60. doi: 10.1002/cne.903120406.

DOI:10.1002/cne.903120406
PMID:1761741
Abstract

Antisera directed against the 48 kDa and 50 kDa cytoskeletal antigens were used to examine changes in the astroglial fabric of the goldfish visual pathways following optic nerve crush. Several major observations are described. First, an optic nerve crush lesion in these animals appears to be devoid of glial cells for at least the first month after surgery. As a corollary, regenerating axons that grow across the lesion may do so over an aglial substrate. Once the axons cross the lesion, their growth is confined to the astroglial domains of the proximal nerve stump. In the optic nerve, gliosis comprises hypertrophy of astrocytic processes such that the open framework characterizing the normal nerve is obscured. In addition, during regeneration, optic nerve glia express large amounts of the 50 kDa cytoskeletal protein, which they ordinarily express at only minimal levels. In the optic tract, gliosis is reflected in a markedly increased expression of the 50 kDa protein as well as an apparent increase in the number and complexity of glial processes. In addition, optic tract glia begin to express the 48 kDa antigen during regeneration. This protein is ordinarily confined for the most part to the optic nerve and is not seen in the tract glia. Finally, no obvious changes were seen in the glia of the optic tectum. These results demonstrate many points of similarity between gliosis in the goldfish and in mammals. However, in some particulars the two responses differ, and it is possible that these differences are related to the differing ability of central axons to regenerate in the two groups of organisms.

摘要

用针对48 kDa和50 kDa细胞骨架抗原的抗血清来检测金鱼视觉通路视神经挤压后星形胶质纤维结构的变化。描述了几个主要观察结果。首先,在这些动物中,视神经挤压损伤在手术后至少第一个月似乎没有神经胶质细胞。相应地,穿过损伤部位生长的再生轴突可能是在无胶质细胞的基质上生长。一旦轴突穿过损伤部位,它们的生长就局限于近端神经残端的星形胶质区域。在视神经中,胶质增生表现为星形胶质细胞突起肥大,从而使正常神经所特有的开放结构变得模糊。此外,在再生过程中,视神经胶质细胞大量表达50 kDa细胞骨架蛋白,而它们通常仅以极低水平表达该蛋白。在视束中,胶质增生表现为50 kDa蛋白的表达明显增加,以及胶质细胞突起的数量和复杂性明显增加。此外,视束胶质细胞在再生过程中开始表达48 kDa抗原。该蛋白通常大部分局限于视神经,在视束胶质细胞中未见。最后,在视顶盖的胶质细胞中未观察到明显变化。这些结果表明金鱼和哺乳动物的胶质增生有许多相似之处。然而,在某些细节上,两种反应有所不同,并且这些差异可能与两组生物体中中枢轴突再生能力的不同有关。

相似文献

1
Gliosis during optic fiber regeneration in the goldfish: an immunohistochemical study.金鱼视神经纤维再生过程中的胶质增生:一项免疫组织化学研究。
J Comp Neurol. 1991 Oct 22;312(4):549-60. doi: 10.1002/cne.903120406.
2
Axon dependent glial changes during optic fiber regeneration in the goldfish.金鱼视神经纤维再生过程中轴突依赖性神经胶质细胞的变化。
J Comp Neurol. 1993 Jul 22;333(4):543-53. doi: 10.1002/cne.903330407.
3
E587 antigen is upregulated by goldfish oligodendrocytes after optic nerve lesion and supports retinal axon regeneration.E587抗原在视神经损伤后被金鱼少突胶质细胞上调,并支持视网膜轴突再生。
Glia. 1998 Jul;23(3):257-70.
4
Organization of astrocytes in the visual pathways of the goldfish: an immunohistochemical study.
J Comp Neurol. 1989 Jul 8;285(2):231-45. doi: 10.1002/cne.902850206.
5
Axonal pathfinding during the regeneration of the goldfish optic pathway.金鱼视觉通路再生过程中的轴突导向
J Comp Neurol. 1989 Jun 1;284(1):119-34. doi: 10.1002/cne.902840109.
6
Axonal regeneration is associated with glial migration: comparison between the injured optic nerves of fish and rats.轴突再生与神经胶质细胞迁移相关:鱼类和大鼠受损视神经的比较。
J Comp Neurol. 1993 Apr 1;330(1):105-12. doi: 10.1002/cne.903300109.
7
Expression of glial fibrillary acidic protein (GFAP) in goldfish optic nerve following injury.损伤后金鱼视神经中胶质纤维酸性蛋白(GFAP)的表达。
Glia. 1990;3(1):33-42. doi: 10.1002/glia.440030106.
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Studies of the early stages of optic axon regeneration in the goldfish.金鱼视神经轴突再生早期阶段的研究。
J Comp Neurol. 1988 May 15;271(3):319-30. doi: 10.1002/cne.902710303.
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Xefiltin, a Xenopus laevis neuronal intermediate filament protein, is expressed in actively growing optic axons during development and regeneration.Xefiltin是一种非洲爪蟾神经元中间丝蛋白,在发育和再生过程中,它在活跃生长的视神经轴突中表达。
J Neurobiol. 1997 Nov 20;33(6):811-24.
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Immunohistochemical localization of CNTFRalpha in adult mouse retina and optic nerve following intraorbital nerve crush: evidence for the axonal loss of a trophic factor receptor after injury.眶内神经挤压后成年小鼠视网膜和视神经中CNTFRalpha的免疫组织化学定位:损伤后营养因子受体轴突损失的证据。
J Comp Neurol. 2007 Jan 10;500(2):384-400. doi: 10.1002/cne.21174.

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