May 2003
Volume 44, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2003
A Rat Model for Non-arteritic Anterior Ischemic Optic Neuropathy
Author Affiliations & Notes
  • H.D. Pomeranz
    Ophthalmology, University of Minnesota, Minneapolis, MN, United States
  • B.A. Ekesten
    Ophthalmology, University of Minnesota, Minneapolis, MN, United States
  • S.L. Bernstein
    Ophthalmology, University of Maryland, Baltimore, MD, United States
  • Footnotes
    Commercial Relationships  H.D. Pomeranz, None; B.A. Ekesten, None; S.L. Bernstein, Patent P.
Investigative Ophthalmology & Visual Science May 2003, Vol.44, 622. doi:
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      H.D. Pomeranz, B.A. Ekesten, S.L. Bernstein; A Rat Model for Non-arteritic Anterior Ischemic Optic Neuropathy . Invest. Ophthalmol. Vis. Sci. 2003;44(13):622.

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

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Abstract

Abstract: : Purpose: Non-arteritic anterior ischemic optic neuropathy (NAION) is a potentially visually devastating disease process in which there is disruption in the arterial blood supply to the optic nerve head, causing ischemic injury to the retinal ganglion axons, resulting in loss of visual field and visual acuity. There are no current effective treatments for this condition. We have validated a rat model for NAION previously reported by Bernstein SL et al (IOVS 42(4), Abstract #5019, 2001) using a different sex and pigmented breed of rat, a different anesthetic system, and skull-implanted electrodes for measuring the visual evoked potential (VEP). Methods: Female Long Evans rats were handled and utilized in accordance with ARVO guidelines. Gold connectors were secured in the skull over the right and left visual cortices. The rats were anesthetized with isofluorane via a nose mask. Flash VEPs and flash electroretinograms (ERG) were measured. After baseline electrophysiological measurements were completed, an intravenous injection of rose bengal was given through a tail vein. An argon green laser beam was directed at the optic nerve head within 1-2 minutes after injection to activate the dye within the arterioles. Gross, histological and electrophysiological techniques were used to determine the extent of damage to the optic nerve. Results: The rat optic disk became edematous within 24 hours after laser treatment. There was no change in ERG measurements before and after laser treatment, supporting the hypothesis that the administration of rose bengal or laser treatment does not damage the retinal circulation in a way that affects the dark- or light-adapted ERGs. Conclusions: The application of argon green laser to the optic disk after administration of rose bengal is a valid animal model for NAION. This method appears to only disturb the vascular supply to the optic nerve and not to the retina as evidenced by normal ERGs before and after laser treatment. This model can be used to test the effectiveness of potential neuroprotective agents on the extent of damage caused by optic nerve ischemia.

Keywords: optic disc • animal model • neuro-ophthalmology: optic nerve 
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