Retinal Ganglion Cell and Nonneuronal Cell Responses to a Microcrush Lesion of Adult Rat Optic Nerve

Sellés-Navarro, Inmaculada; Ellezam, Benjamin; Fajardo, Raúl; Latour, Mathieu; McKerracher, Lisa

doi:10.1006/exnr.2000.7573

Cited by 126 publications

(87 citation statements)

References 38 publications

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“…We did not find a lesion-induced increase in CS immunoreactivity in the optic nerve of zebrafish, whereas in the optic nerve (Selles-Navarro et al, 2001) and spinal cord of mammals (Davies et al, 1997(Davies et al, , 1999Pasterkamp et al, 2001), detectability of CSs and their core proteins (Levine, 1994;McKeon et al, 1999) is strongly increased after a lesion. However, increased expression of CSs in the injured optic nerve of the goldfish, which is closely related to zebrafish, has been described previously (Battisti et al, 1992).…”

Section: Discussioncontrasting

confidence: 78%

Repellent Guidance of Regenerating Optic Axons by Chondroitin Sulfate Glycosaminoglycans in Zebrafish

Becker

2002

J. Neurosci.

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We analyzed the role of chondroitin sulfate (CS) glycosaminoglycans, putative inhibitors of axonal regeneration in mammals, in the regenerating visual pathway of adult zebrafish. In the adult, CS immunoreactivity was not detectable before or after an optic nerve crush in the optic nerve and tract but was constitutively present in developing and adult nonretinorecipient pretectal brain nuclei, where CSs may form a boundary preventing regenerating optic fibers from growing into these inappropriate locations. Enzymatic removal of CSs by chondroitinase ABC after optic nerve crush significantly increased the number of animals showing erroneous growth of optic axons into the nonretinorecipient magnocellular superficial/ posterior pretectal nucleus (83% vs 42% in controls). In vitro, a substrate border of CSs, but not heparan sulfates, strongly repelled regenerating retinal axons from adult zebrafish. We conclude that CSs contribute to repellent axon guidance during regeneration of the optic projection in zebrafish.

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Section: Discussioncontrasting

confidence: 78%

Repellent Guidance of Regenerating Optic Axons by Chondroitin Sulfate Glycosaminoglycans in Zebrafish

Becker

2002

J. Neurosci.

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“…CSPGs can actively inhibit neurite outgrowth and neural regeneration after CNS injury as well as function as a physical barrier [35][36][37][38][39]. CSPGs consist of a protein core and covalently coupled glycosaminoglycans (CS-GAGs).…”

Section: Discussionmentioning

confidence: 99%

GM-CSF inhibits glial scar formation and shows long-term protective effect after spinal cord injury

Huang

Kim

Kong

et al. 2009

Journal of the Neurological Sciences

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“…Intraorbital microlesions effectively axotomize all RGC axons and provide a welldefined lesion site (Selles-Navarro et al, 2001). Microlesions were performed on female Sprague Dawley rats (180 -200 g; Charles River, StConstant, Québec, Canada) under gas anesthesia with 2.5-3% isoflurane in oxygen.…”

Section: Methodsmentioning

confidence: 99%

Application of Rho Antagonist to Neuronal Cell Bodies Promotes Neurite Growth in Compartmented Cultures and Regeneration of Retinal Ganglion Cell Axons in the Optic Nerve of Adult Rats

Bertrand¹,

Winton²,

et al. 2005

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Inactivation of Rho promotes neurite growth on inhibitory substrates and axon regeneration in vivo.Here, we compared axon growth when neuronal cell bodies or injured axons were treated with a cell-permeable Rho antagonist (C3-07) in vitro and in vivo. In neurons plated in compartmented cultures, application of C3-07 to either cell bodies or distal axons promoted axonal growth on myelinassociated glycoprotein substrates. In vivo, an injection of C3-07 into the eye promoted regeneration of retinal ganglion cell (RGC) axons in the optic nerve after microcrush lesion. Delayed application of C3-07 promoted RGC growth across the lesion scar. Application of C3-07 completely prevented RGC cell death for 1 week after axotomy. To investigate the mechanism by which Rho inactivation promotes RGC growth, we studied slow axonal transport. Reduction in slow transport of cytoskeletal proteins was observed after axotomy, but inactivation of Rho did not increase slow axonal transport rates. Together, our results indicate that application of a Rho antagonist at the cell body is neuroprotective and overcomes growth inhibition but does not fully prime RGCs for active growth.

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Retinal Ganglion Cell and Nonneuronal Cell Responses to a Microcrush Lesion of Adult Rat Optic Nerve

Cited by 126 publications

References 38 publications

Repellent Guidance of Regenerating Optic Axons by Chondroitin Sulfate Glycosaminoglycans in Zebrafish

Repellent Guidance of Regenerating Optic Axons by Chondroitin Sulfate Glycosaminoglycans in Zebrafish

GM-CSF inhibits glial scar formation and shows long-term protective effect after spinal cord injury

Application of Rho Antagonist to Neuronal Cell Bodies Promotes Neurite Growth in Compartmented Cultures and Regeneration of Retinal Ganglion Cell Axons in the Optic Nerve of Adult Rats

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