May 2003
Volume 44, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2003
Establishment of an Animal Model for Acute Glaucoma: The Need for Immune Modulation as a Therapeutic Strategy
Author Affiliations & Notes
  • G.J. Ben Simon
    Neurobiology, Weizmann institute of Science, Rehovot, Israel
  • S. Bakalash
    Neurobiology, Weizmann Institute of Science, Rehovot, Israel
  • E. Aloni
    Neurobiology, Weizmann institute of science, Rehovot, Israel
  • M. Schwartz
    Neurobiology, Weizmann institute of science, Rehovot, Israel
  • Footnotes
    Commercial Relationships  G.J. Ben Simon, None; S. Bakalash, None; E. Aloni, None; M. Schwartz, None.
  • Footnotes
    Support  none
Investigative Ophthalmology & Visual Science May 2003, Vol.44, 112. doi:
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      G.J. Ben Simon, S. Bakalash, E. Aloni, M. Schwartz; Establishment of an Animal Model for Acute Glaucoma: The Need for Immune Modulation as a Therapeutic Strategy . Invest. Ophthalmol. Vis. Sci. 2003;44(13):112.

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

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Abstract

Abstract: : Purpose: To establish a rat model that simulates acute glaucoma in terms of retinal ganglion cell (RGC) death and the window for therapeutic vaccination with Cop-1. Methods: High intraocular pressure (IOP) was induced unilaterally in deeply anesthetized SPD rats by inserting a 30-gauge needle connected to a polyethylene tube through which normal saline (0.9%) in a bag held 1 meter above the rat's head was infused for 1 hour into the anterior chamber of the eye. IOP was assessed using a Tono-Pen tonometer (XL, Mentor¨). RGC survival 1 and 2 weeks after the high-pressure insult was assessed by counting the RGCs that had been retrogradely labeled with rhodamine dextran. Results: Saline infusion for 1 hour increased the IOP from 19(±4) to 44(±11) mm Hg. Baseline IOP values were restored after 24 hours. By 1 week after IOP insult, the RGC count had decreased by 30%. Vaccination with Cop-1 on the day of the insult prevented 50% of the IOP-induced RGC loss. Protection by Cop-1 was effective even if the vaccination was administered as late as 3 days after the insult. Conclusions: Raising the IOP to 44 mmHg for 1 hour causes death of RGCs in rats. Significant protection of RGCs from the IOP-induced death can be achieved by a single immunization with Cop-1. At least 50% of the potentially doomed RGCs can be rescued, suggesting that in the absence of treatment not all of the neuronal death in this model is a direct result of the IOP insult, but some neurons die because of the insult-induced hostility of the extracellular environment. These findings may have immediate application as a basis for glaucoma therapy, as Cop-1 (administered according to a different protocol) a clinically approved drug for multiple sclerosis.

Keywords: immunomodulation/immunoregulation 
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