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Quantitating Pressure-Induced Optic Nerve Injury In A Rat Model Of Glaucoma.

Published online by Cambridge University Press:  02 July 2020

E.C. Johnson ,
W.O. Cepurna  and
J.C. Morrison
E.C. Johnson
Affiliation:
Casey Eye Institute, Oregon Health Sciences University, Portland, Oregon97201.
W.O. Cepurna
Affiliation:
Casey Eye Institute, Oregon Health Sciences University, Portland, Oregon97201.
J.C. Morrison
Affiliation:
Casey Eye Institute, Oregon Health Sciences University, Portland, Oregon97201.
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Extract

Elevated intraocular pressure (IOP) is the most widely recognized risk factor for glaucoma and the target of nearly all current glaucoma therapy. The goal of our laboratory is to understand mechanism by which elevated IOP results in axonal degeneration in the optic nerve.

In order to study the effects of IOP level on the optic nerve, we have developed a number of methods to modulate IOP in the rat. We sclerose the aqueous humor outflow pathways to elevate IOP for a period of weeks to produce focal optic nerve lesions. This method reproduces many of the pathological characteristics of human glaucoma. A modification of this method uses constant light (CL) housing to stabilize the normally wide circadian IOP oscillations, simplifying the correlation of IOP history with lesion size. However, the CL-stabilized IOP in untreated, fellow eyes is above the normal light phase IOP of 20 mm Hg and close to the normal dark, phase value of 30 mm Hg.

Type
Highlights Of Biological Microscopy In The Pacific Northwest Usa
Information
Microscopy and Microanalysis , Volume 5 , Issue S2: Proceedings: Microscopy & Microanalysis '99, Microscopy Society of America 57th Annual Meeting, Microbeam Analysis Society 33rd Annual Meeting, Portland, Oregon August 1-5, 1999 , August 1999 , pp. 1224 - 1225
Copyright
Copyright © Microscopy Society of America

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References

Reference:

Morrison, JC, Moore, CG, EC, Johnson, Deppmeier, LMH, Meshul, C, Gold, BG: A rat model of chronic pressure-induced optic nerve damage. Exp Eye Res. 1997;64:85–96.CrossRefGoogle ScholarPubMed