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Conference Paper: Regeneration of optic nerve

TitleRegeneration of optic nerve
Authors
Issue Date2011
PublisherPion Ltd.. The Journal's web site is located at http://i-perception.perceptionweb.com/journal/I/
Citation
The 7th Asia-Pacific Conference on Vision (APCV 2011), Hong Kong, 15-18 July 2011. In i-Perception, 2011, v. 2 n. 4, p. 235 How to Cite?
AbstractThe 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.
Description2011 亞太視覺會議
Keynote
Open Access Journal
Persistent Identifierhttp://hdl.handle.net/10722/140043
ISSN

 

DC FieldValueLanguage
dc.contributor.authorSo, KFen_US
dc.date.accessioned2011-09-23T06:05:26Z-
dc.date.available2011-09-23T06:05:26Z-
dc.date.issued2011en_US
dc.identifier.citationThe 7th Asia-Pacific Conference on Vision (APCV 2011), Hong Kong, 15-18 July 2011. In i-Perception, 2011, v. 2 n. 4, p. 235en_US
dc.identifier.issn2041-6695-(electronic)-
dc.identifier.urihttp://hdl.handle.net/10722/140043-
dc.description2011 亞太視覺會議-
dc.descriptionKeynote-
dc.descriptionOpen Access Journal-
dc.description.abstractThe 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.-
dc.languageengen_US
dc.publisherPion Ltd.. The Journal's web site is located at http://i-perception.perceptionweb.com/journal/I/-
dc.relation.ispartofi-Perceptionen_US
dc.titleRegeneration of optic nerveen_US
dc.typeConference_Paperen_US
dc.identifier.emailSo, KF: hrmaskf@hku.hken_US
dc.description.naturelink_to_OA_fulltext-
dc.identifier.hkuros195371en_US
dc.identifier.volume2-
dc.identifier.issue4-
dc.identifier.spage235en_US
dc.identifier.epage235en_US
dc.publisher.placeUnited Kingdom-
dc.description.otherThe 7th Asia-Pacific Conference on Vision (APCV 2011), Hong Kong, 15-18 July 2011. In i-Perception, 2011, v. 2 n. 4, p. 235-

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