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Type: Conference paper
Title: Evaluation of Axonal Regeneration in a Rat Model of Experimental Glaucoma
Author: Chidlow, G.
Wood, J.
Ebneter, A.
Casson, R.
Citation: ARVO 2011 Annual Meeting - Abstracts by Scientific Section/Group - Glaucoma (GL), 2011 / vol.52, pp.2453
Publisher: Assoc Research Vision Ophthalmology Inc
Publisher Place: 12300 Twinbrook Parkway, Rockville, USA, Md, 20852-1606
Issue Date: 2011
Conference Name: Association of Research Vision Ophthalmology Annual Meeting (01 Jun 2010 : Investigative Ophthalmology & Visual Science)
Statement of
Glyn Chidlow, John P. Wood, Andreas Ebneter, Robert J. Casson
Abstract: Purpose: Axonal injury in the CNS is not followed by any beneficial regeneration. After traumatic injuries such as optic nerve (ON) transection or crush, retinal ganglion cell (RGC) axons display transient, local sprouting proximal to the site of damage, but fail to regenerate beyond the lesion site. Unlike traumatic ON injuries, RGCs are lost gradually during experimental glaucoma and only a proportion will die; moreover, the locus of injury to RGCs is unclear. In the current study, we investigated RGC regeneration, as delineated by Gap43 outgrowth and protein level, in a rat model of experimental glaucoma. Methods: Experimental glaucoma was induced in one eye by lasering the trabecular meshwork to chronically elevate the intraocular pressure. Other rats received ON crush. Rats were killed at various time points. Eyes with optic nerve attached were carefully dissected, fixed in buffered formalin, embedded in paraffin and 4μm thick sections taken. Sections were then processed for immunohistochemistry. Western blotting was performed using a standard methodology. Results: In normal rats, negligible Gap43 immunoreactivity was associated with RGC bodies or their axons. At 24h after induction of raised IOP, widespread axonal transport disruption was observed at the ONH, as determined by APP immunostaining, but no increase in Gap43. By 3d, limited Gap43 immunohistochemistry was detectable in RGC axons of some rats, particularly at the level of the prelaminar ONH, while Western blotting showed an upregulated level of retinal Gap43 protein. The expression of Gap43 increased further at 7d and 14d, as evidenced by immunohistochemistry and Western blotting. The pattern of Gap43 immunoreactivity in ocular hypertensive rats was broadly equivalent to that of APP with accumulation throughout the ONH, but was significantly delayed in onset. While APP immunostaining was maximal at 1d and then gradually declined over 14d, the opposite occurred for Gap43. Unlike APP, a few Gap43-positive axons extended beyond the ONH into the initial myelinated portion of the ON and small punctae of Gap43 immunoreactivity were apparent in the distal ON and OT. Nevertheless, Western blotting showed no measureable increase in the Gap43 content of the myelinated ON at 7d. Conclusions: The overall results indicate that limited axonal regeneration occurs during experimental glaucoma, but does not generally proceed beyond the ONH. This finding provides further evidence that the ONH is the principal site of axonal injury and that chronically raised IOP induces a crush-like insult at this location.
Rights: Copyright status unknown
RMID: 0020119098
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Appears in Collections:Opthalmology & Visual Sciences publications

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