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Open AccessJournal ArticleDOI

Regional Retinal Ganglion Cell Axon Loss in a Murine Glaucoma Model.

TLDR
There was selectively greater loss of superior and temporal optic nerve axons of RGCs in mouse glaucoma at certain stages of damage, suggesting non-RGC responses differ between mouse strains.
Abstract
Purpose To determine if retinal ganglion cell (RGC) axon loss in experimental mouse glaucoma is uniform in the optic nerve. Methods Experimental glaucoma was induced for 6 weeks with a microbead injection model in CD1 (n = 78) and C57BL/6 (B6, n = 68) mice. From epoxy-embedded sections of optic nerve 1 to 2 mm posterior to the globe, total nerve area and regional axon density (axons/1600 μm2) were measured in superior, inferior, nasal, and temporal zones. Results Control eyes of CD1 mice have higher axon density and more total RGCs than control B6 mice eyes. There were no significant differences in control regional axon density in all mice or by strain (all P > 0.2, mixed model). Exposure to elevated IOP caused loss of RGC in both strains. In CD1 mice, axon density declined without significant loss of nerve area, while B6 mice had less density loss, but greater decrease in nerve area. Axon density loss in glaucoma eyes was not significantly greater in any region in either mouse strain (both P > 0.2, mixed model). In moderately damaged CD1 glaucoma eyes, and CD1 eyes with the greatest IOP elevation exposure, density loss differed by region (P = 0.05, P = 0.03, mixed model) with the greatest loss in the temporal and superior regions, while in severely injured B6 nerves superior loss was greater than inferior loss (P = 0.01, mixed model, Bonferroni corrected). Conclusions There was selectively greater loss of superior and temporal optic nerve axons of RGCs in mouse glaucoma at certain stages of damage. Differences in nerve area change suggest non-RGC responses differ between mouse strains.

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Neuroprotective strategies for retinal disease.

TL;DR: Six strategies that preserve retinal neurons across multiple diseases are presented, including drugs that target survival pathways, therapies that target retinal dopamine, and neurotrophic factors, and rehabilitative methods that increase endogenous repair mechanisms, including exercise and electrical stimulation therapies.
Journal ArticleDOI

Recent advances in genetically modified animal models of glaucoma and their roles in drug repositioning.

TL;DR: The benefits and limitations of using disease models of glaucoma and recent basic research in retinal protection using existing drugs are summarized.
Journal ArticleDOI

Review of rodent hypertensive glaucoma models

TL;DR: The outcomes of induced rodent hypertensive glaucoma models including intracameral injection of microbeads, laser photocoagulation, episcleral vein cauterization, injection of hypertonic saline and hyaluronic acid are summarized.
Journal ArticleDOI

TRPA1 mediates damage of the retina induced by ischemia and reperfusion in mice

TL;DR: Findings suggest that TRPA1 mediates the oxidative stress burden and inflammation that result in murine retinal cell death and it is possible that inhibition of a TRPA 1-dependent pathway could also attenuate glaucoma-related retinal damage.
Journal ArticleDOI

Comparative analysis of retinal ganglion cell damage in three glaucomatous rat models.

TL;DR: This study provides detailed data for choosing suitable animal models to advance glaucomatous rat models and found that the PhNR amplitudes declined early by the first day in the NMDA group, 5 days later in the EVC group and by 7 days in the microbead group.
References
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Journal ArticleDOI

Optic Nerve Damage in Human Glaucoma: III. Quantitative Correlation of Nerve Fiber Loss and Visual Field Defect in Glaucoma, Ischemic Neuropathy, Papilledema, and Toxic Neuropathy

TL;DR: The pattern of atrophy in examples of toxic amblyopia, ischemic optic neuropathy and chronic papilledema differ from that of glaucoma, suggesting different mechanisms of damage in these conditions.
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The optic nerve head as a biomechanical structure: a new paradigm for understanding the role of IOP-related stress and strain in the pathophysiology of glaucomatous optic nerve head damage.

TL;DR: Modeling the ONH as a biomechanical structure generates a group of testable hypotheses regarding the central mechanisms of glaucomatous damage and provides a logic for classifying the principal components of the susceptibility of an individual ONH to a given level of IOP.
Journal Article

Retinal ganglion cell death in experimental glaucoma and after axotomy occurs by apoptosis.

TL;DR: Some retinal ganglion cells injured by glaucoma and by axotomy die by apoptosis, possibly because of the small proportion of cells that were dying at any given time.
Journal ArticleDOI

Regional Differences in the Structure of the Lamina Cribrosa and Their Relation to Glaucomatous Optic Nerve Damage

TL;DR: Using a new technique for scanning electron microscopic examination of human optic nerve heads, regional differences were found in the fine structure of the lamina cribrosa that may explain the characteristic pattern of early glaucomatous field loss.
Journal ArticleDOI

Predictive factors for glaucomatous visual field progression in the Advanced Glaucoma Intervention Study.

TL;DR: Both increasing age and greater IOP fluctuation increase the odds of VF progression by 30% (for each 5-year increment in age and 1-mmHg increase in IOP fluctuations), and the higher risk conferred by Iop fluctuation was consistently observed in eyes with and without a history of cataract extraction.
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