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Diego Fernandez, Damian Dorfman, Ruth Rosenstein; Ischemic conditioning protects from axoglial alterations of the optic pathway induced by experimental diabetes in rats. Invest. Ophthalmol. Vis. Sci. 2013;54(15):3245.
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Diabetic retinopathy is a leading cause of blindness. Visual function disorders have been demonstrated in diabetics even before the onset of retinopathy. At early stages of experimental diabetes, axoglial alterations occur at the distal portion of the optic nerve. Although ischemic conditioning can protect neurons against ischemic damage, there is no information on its ability to protect axons. We analyzed the effect of ischemic conditioning on the early axoglial alterations in the distal portion of the optic nerve induced by experimental diabetes.
Diabetes was induced in Wistar rats by an intraperitoneal injection of streptozotocin. Retinal ischemia was induced by increasing intraocular pressure to 120 mm Hg for 5 min; this maneuver started 3 days after streptozotocin injection and was weekly repeated in one eye, while the contralateral eye was submitted to a sham procedure. After 6 weeks of diabetes induction, the effect of ischemic conditioning was evaluated using different morphological techniques. At this time point, the activity of glutamine synthetase was also evaluated in all the experimental groups.
The application of ischemia pulses prevented the deficit in the anterograde transport of cholera toxin β subunit (CTB) from the retina to the superior colliculus, as well as the increase in astrocyte reactivity, ultraestructural myelin alterations, and altered morphology of oligodendrocyte lineage in the optic nerve distal portion induced by streptozotocin injection. Ischemia tolerance prevented a significant decrease of retinal glutamine synthetase activity induced by diabetes.
These results suggest that early vision loss in diabetes could be abated by ischemic conditioning which preserved axonal function and structure.
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