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This Article Full Text Full Text (PDF) All Versions of this Article: iovs.09-4324v1 51/2/980    most recent Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Fu, C. T. Articles by Sretavan, D. PubMed PubMed Citation Articles by Fu, C. T. Articles by Sretavan, D.

Laser-Induced Ocular Hypertension in Albino CD-1 Mice

From the ¹Neuroscience Graduate Program and the Departments of ²Ophthalmology and ³Physiology, University of California, San Francisco, San Francisco, California.

Corresponding author: Christine T. Fu, Department of Ophthalmology, University of California, San Francisco, Box 0730, 10 Koret Way, San Francisco, CA 94143; cfu{at}vision.ucsf.edu.

Purpose. To establish a laser-induced model of ocular hypertension (LIOH) in albino CD-1 mice and to characterize the sequence of pathologic events triggered by intraocular pressure (IOP) elevation.

Methods. LIOH was induced unilaterally in CD-1 mice by laser photocoagulation of limbal and episcleral veins 270° to 300° circumferentially, sparing the nasal aspect and the long ciliary arteries. IOP was measured with a rebound tonometer. Hematoxylin and eosin-stained plastic sections were used for morphometric analysis of retinal layers, and retinal whole-mounts were immunostained with anti-Brn-3b to quantify retinal ganglion cell (RGC) gene expression ion and density. Axonal and myelin morphologies were characterized using appropriate antibodies, and axon counts were obtained from paraphenylenediamine-stained optic nerve sections.

Results. LIOH resulted in IOP doubling within 4 hours after laser treatment, which returned to normal by 7 days. Axon degenerative changes, reactive plasticity, and aberrant regrowth were detected at the optic nerve head (ONH) as early as 4 days after treatment. By 7 days, axon number was significantly reduced in the myelinated optic nerve, with concurrent signs of myelin degradation. At 14 days, Brn-3b⁺ RGC density was reduced, with neuronal loss confined to the RGC layer and no apparent effects on other retinal layers.

Conclusions. Laser photocoagulation of limbal and episcleral veins induces transient ocular hypertension in albino CD-1 mice. The ensuing retinal and optic nerve pathologic events recapitulated key features of glaucoma and placed ONH RGC axon responses as an early manifestation of damage. LIOH in albino mice may be useful as a mouse model to examine mechanisms of RGC and axon glaucomatous injury.