April 2010
Volume 51, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2010
Intraocular Pressure Elevation Stimulates Successful Regeneration of Retinal Ganglion Cell Axons in vivo After Optic Nerve Crush in Adult Rats
Author Affiliations & Notes
  • B. Lorber
    Centre for Brain Repair, Department of Ophthalmology, University of Cambridge, Cambridge, United Kingdom
  • A. Guidi
    Centre for Brain Repair, Department of Ophthalmology, University of Cambridge, Cambridge, United Kingdom
  • K. R. Martin
    Centre for Brain Repair, Department of Ophthalmology, University of Cambridge, Cambridge, United Kingdom
  • Footnotes
    Commercial Relationships  B. Lorber, None; A. Guidi, None; K.R. Martin, None.
  • Footnotes
    Support  Glaucoma Research Foundation, GSK Clinician Scientist Fellowship Programme, Richard Norden Glaucoma Research Fund
Investigative Ophthalmology & Visual Science April 2010, Vol.51, 5218. doi:
  • Views
  • Share
  • Tools
    • Alerts
      ×
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      B. Lorber, A. Guidi, K. R. Martin; Intraocular Pressure Elevation Stimulates Successful Regeneration of Retinal Ganglion Cell Axons in vivo After Optic Nerve Crush in Adult Rats. Invest. Ophthalmol. Vis. Sci. 2010;51(13):5218.

      Download citation file:


      © ARVO (1962-2015); The Authors (2016-present)

      ×
  • Supplements
Abstract

Purpose: : Elevation of intraocular pressure (IOP) reduces retinal ganglion cell (RGC) survival in human glaucoma and experimental animal models. We recently showed that IOP elevation enhances RGC neurite outgrowth in culture, an effect mediated by activated retinal glia. We therefore investigated if IOP elevation would also lead to successful RGC axon regeneration after optic nerve crush (ONC) in adult rats in vivo.

Methods: : Adult Sprague Dawley-rats received (a) unilateral ONC (n=8), (b) IOP elevation using a trabecular laser model (n=8), (c) ONC+IOP elevation (n=7), or were left untreated (n=8). RGC survival (Nr. of βIII-tubulin/NeuN+ RGC) and retinal glia activation (intensity of GFAP labeling) were quantified in retinal sections 14 days later. The number of GAP43+ RGC axons regenerating past the optic nerve lesion site was also assessed.

Results: : RGC survival vs. controls was 56±1.7% after ONC (p<0.001) and 87.3±6% after IOP elevation (p<0.05). Combination of ONC+IOP elevation led to survival of 62.4±3.2% RGC vs. untreated controls (p<0.001), a slight, but significant increase in survival vs. ONC alone (p<0.05). Therefore, ONC+IOP elevation did not result in enhanced RGC death over single treatment, as might be expected. ONC slightly increased retinal glia activation vs. controls (8.6±3.8%), whilst retinal glia activation was higher after IOP elevation (20.2±5.2%; p<0.01 vs. controls, p<0.05 vs. ONC). ONC+IOP strongly increased retinal glia activation (38.1±4.2%) over ONC (p<0.001) and IOP elevation (p<0.05). Concurrently, whilst after ONC only few GAP43+ axons grew past the optic nerve lesion site (21.9±9.2), ONC+IOP elevation led to a ~10 fold increase (203.4±24.1; p<0.001) in regenerating GAP43+ axons.

Conclusions: : Acute IOP elevation at the time of ONC led to strongly enhanced retinal glia activation compared to ONC alone. This correlated with a strong increase in RGC axon regeneration potential, and also a slight increase in RGC survival over ONC. These results suggest that enhancing retinal glia activation may facilitate neuronal survival and axon regeneration after injury/disease.

Keywords: regeneration • retina • glia 
×
×

This PDF is available to Subscribers Only

Sign in or purchase a subscription to access this content. ×

You must be signed into an individual account to use this feature.

×