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Regeneration of Optic Nerve

The optic nerve is part of the central nervous system (CNS) and has a structure similar to other CNS tracts. The axons that form the optic nerve originate in the ganglion cell layer of the retina and extend through the optic tract. As a tissue, the optic nerve has the same organization as the white...

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Autor principal: So, Kwok-Fai
Formato: Online Artículo Texto
Lenguaje:English
Publicado: SAGE Publications 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5393758/
http://dx.doi.org/10.1068/ic235
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author So, Kwok-Fai
author_facet So, Kwok-Fai
author_sort So, Kwok-Fai
collection PubMed
description The optic nerve is part of the central nervous system (CNS) and has a structure similar to other CNS tracts. The axons that form the optic nerve originate in the ganglion cell layer of the retina and extend through the optic tract. As a tissue, the optic nerve has the same organization as the white matter of the brain in regard to its glia. There are three types of glial cells: Oligodendrocytes, astrocytes, and microglia. Little structural and functional regeneration of the CNS takes place spontaneously following injury in adult mammals. In contrast, the ability of the mammalian peripheral nervous system (PNS) to regenerate axons after injury is well documented. A number of factors are involved in the lack of CNS regeneration, including: (i) the response of neuronal cell bodies against the damage; (ii) myelin-mediated inhibition by oligodendrocytes; (iii) glial scarring, by astrocytes; (iv) macrophage infiltration; and (v) insufficient trophic factor support. The fundamental difference in the regenerative capacity between CNS and PNS neuronal cell bodies has been the subject of intensive research. In the CNS the target normally conveys a retrograde trophic signal to the cell body. CNS neurons die because of trophic deprivation. Damage to the optic nerve disconnects the neuronal cell body from its target-derived trophic peptides, leading to the death of retinal ganglion cells. Furthermore, the axontomized neurons become less responsive to the peptide trophic signals they do receive. On the other hand, adult PNS neurons are intrinsically responsive to neurotrophic factors and do not lose trophic responsiveness after axotomy. In this talk different strategies to promote optic-nerve regeneration in adult mammals are reviewed. Much work is still needed to resolve many issues. This is a very important area of neuroregeneration and neuroprotection, as currently there is no cure after traumatic optic nerve injury or retinal disease such as glaucoma, which affect retinal ganglion cells and optic nerve axons.
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spelling pubmed-53937582017-04-24 Regeneration of Optic Nerve So, Kwok-Fai Iperception Article The optic nerve is part of the central nervous system (CNS) and has a structure similar to other CNS tracts. The axons that form the optic nerve originate in the ganglion cell layer of the retina and extend through the optic tract. As a tissue, the optic nerve has the same organization as the white matter of the brain in regard to its glia. There are three types of glial cells: Oligodendrocytes, astrocytes, and microglia. Little structural and functional regeneration of the CNS takes place spontaneously following injury in adult mammals. In contrast, the ability of the mammalian peripheral nervous system (PNS) to regenerate axons after injury is well documented. A number of factors are involved in the lack of CNS regeneration, including: (i) the response of neuronal cell bodies against the damage; (ii) myelin-mediated inhibition by oligodendrocytes; (iii) glial scarring, by astrocytes; (iv) macrophage infiltration; and (v) insufficient trophic factor support. The fundamental difference in the regenerative capacity between CNS and PNS neuronal cell bodies has been the subject of intensive research. In the CNS the target normally conveys a retrograde trophic signal to the cell body. CNS neurons die because of trophic deprivation. Damage to the optic nerve disconnects the neuronal cell body from its target-derived trophic peptides, leading to the death of retinal ganglion cells. Furthermore, the axontomized neurons become less responsive to the peptide trophic signals they do receive. On the other hand, adult PNS neurons are intrinsically responsive to neurotrophic factors and do not lose trophic responsiveness after axotomy. In this talk different strategies to promote optic-nerve regeneration in adult mammals are reviewed. Much work is still needed to resolve many issues. This is a very important area of neuroregeneration and neuroprotection, as currently there is no cure after traumatic optic nerve injury or retinal disease such as glaucoma, which affect retinal ganglion cells and optic nerve axons. SAGE Publications 2011-05-01 2011-05 /pmc/articles/PMC5393758/ http://dx.doi.org/10.1068/ic235 Text en © 2011 SAGE Publications Ltd. Manuscript content on this site is licensed under Creative Commons Licenses http://creativecommons.org/licenses/by-nc-nd/3.0/ This article is distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs 3.0 License (http://www.creativecommons.org/licenses/by-nc-nd/3.0/) which permits non-commercial use, reproduction and distribution of the work as published without adaptation or alteration, without further permission provided the original work is attributed as specified on the SAGE and Open Access page (http://www.uk.sagepub.com/aboutus/openaccess.htm).
spellingShingle Article
So, Kwok-Fai
Regeneration of Optic Nerve
title Regeneration of Optic Nerve
title_full Regeneration of Optic Nerve
title_fullStr Regeneration of Optic Nerve
title_full_unstemmed Regeneration of Optic Nerve
title_short Regeneration of Optic Nerve
title_sort regeneration of optic nerve
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5393758/
http://dx.doi.org/10.1068/ic235
work_keys_str_mv AT sokwokfai regenerationofopticnerve