March 2012
Volume 53, Issue 14
ARVO Annual Meeting Abstract  |   March 2012
A Novel Rodent Model of Posterior Ischemic Optic Neuropathy
Author Affiliations & Notes
  • Yan Wang
    Ophthalmology, Bascom Palmer Eye Institute, Miami, Florida
  • Dale Brown
    Neuroscience, University of Miami, Miami, Florida
  • Brant Watson
    Department of Neurology, University of Miami Miller School of Medicine, Miami, Florida
  • Yuanli Duan
    Ophthalmology, Bascom Palmer Eye Institute, Miami, Florida
  • Jeffrey L. Goldberg
    Ophthalmology, Bascom Palmer Eye Institute, Miami, Florida
  • Footnotes
    Commercial Relationships  Yan Wang, None; Dale Brown, None; Brant Watson, None; Yuanli Duan, None; Jeffrey L. Goldberg, None
  • Footnotes
    Support  the American Heart Association (JLG); the James and Esther King Biomedical Research Program (JLG); NEI P30 Core Grant EY014801;
Investigative Ophthalmology & Visual Science March 2012, Vol.53, 2977. doi:
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      Yan Wang, Dale Brown, Brant Watson, Yuanli Duan, Jeffrey L. Goldberg; A Novel Rodent Model of Posterior Ischemic Optic Neuropathy. Invest. Ophthalmol. Vis. Sci. 2012;53(14):2977.

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

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Purpose: : Posterior Ischemic optic neuropathy (PION) is a sight devastating disease in clinical practice. However its pathogenesis and natural history has remained poorly understood. The purpose of this study was to develop a reliable, reproducible animal model of PION and test the treatment effect of neurotrophic factors on PION model.

Methods: : PION was induced in adult Sprague-Dawley rats by illuminating the posterior portion of optic nerve with Nd:YAG laser immediately after intravenous injection of erythrosine B (EB). The integrity of the circulation in the retina and optic nerve was examined by FITC-dextran extravasation 1 hour after PION induction. The histopathologic and inflammatory changes of the optic nerve were characterized by H&E and ED1 immunostaining. RGC survival at different time points after PION induction, with or without neurotrophic application, was quantified by counting the number of Fluorogold retrograde-labeled RGCs in retina flat mounts.

Results: : Fluorescein dye leakage was observed in the lesion area of the optic nerve one hour after PION induction. The lesion area of the optic nerve became edematous 3 days post injury and then underwent cavernous degeneration. ED1 positive microglia/macrophages first appeared in the lesion area and migrated to the distal portion of optic nerve as well as optic chiasm. RGCs died in a time dependent manner and around 30% RGCs survived 3 weeks post injury. Multiple application of BDNF or CNTF, however, could rescue RGC survival up to 70% 3 weeks post injury.

Conclusions: : The retinal and optic nerve changes occurring after PION induction were similar to key features of human PION. Our model provides a novel platform for future research on detailed pathogenesis and molecular changes in PION; and can be further optimized for pre-clinical drug screening of interventional agents against PION as well as other CNS ischemic disease.

Keywords: ischemia • apoptosis/cell death • neuroprotection 

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