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|Title:||Protection of retinal ganglion cells and the optic nerve during short-term hyperglycemia in experimental glaucoma|
|Citation:||Archives of Ophthalmology, 2011; 129(10):1337-1344|
|Publisher:||Amer Medical Assoc|
|Andreas Ebneter, Glyn Chidlow, John P. M. Wood, Robert J. Casson|
|Abstract:||Objective: To evaluate the neuroprotective effect of short-term hyperglycemia on the retinal ganglion cell body and axon in a rat model of experimental glaucoma. Methods: Using a well-described limbal laser technique, unilateral ocular hypertension was induced in 2 groups (26 per group) of Sprague-Dawley rats. One group remained normoglycemic; the other was rendered hyperglycemic by means of an intraperitoneal injection of streptozocin. After 2 weeks of elevated intraocular pressure, axonal and retinal damage profiles were compared using several histological techniques. Immunohistochemical changes in the retina and optic nerve were also assessed. Results: We found convincing evidence of delayed axonal degeneration and retinal ganglion cell death in hyperglycemic rats. Axon loss was reduced by about 50% 2 weeks after induction of ocular hypertension. Survival of retinal ganglion cell perikarya increased to a similar extent in hyperglycemic rats. Conclusions: The optic nerve and retinal ganglion cells are partially protected by short-term hyperglycemia in this rat model of experimental glaucoma. Energy substrate availability may therefore play a role in glaucomatous optic neuropathy.|
|Keywords:||Axons; Retinal Ganglion Cells; Animals; Rats; Rats, Sprague-Dawley; Optic Nerve Diseases; Ocular Hypertension; Diabetes Mellitus, Experimental; Hyperglycemia; Nerve Degeneration; Blood Glucose; Nerve Tissue Proteins; Biological Markers; Tonometry, Ocular; Cell Count; Immunohistochemistry; Cell Survival; Intraocular Pressure; Cytoprotection|
|Rights:||©2011 American Medical Association. All rights reserved.|
|Appears in Collections:||Opthalmology & Visual Sciences publications|
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