title: Ischemic conditioning protects from axoglial alterations of the optic pathway induced by experimental diabetes in rats.
abstract: 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 and synaptic terminals 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. The application of ischemia pulses prevented a deficit in the anterograde transport from the retina to the superior colliculus, as well as an increase in astrocyte reactivity, ultraestructural myelin alterations, and altered morphology of oligodendrocyte lineage in the optic nerve distal portion at early stages of experimental diabetes. 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.
authors.affiliation: Laboratory of Retinal Neurochemistry and Experimental Ophthalmology, Department of Human Biochemistry, School of Medicine, University of Buenos Aires/CEFyBO, CONICET, Buenos Aires, Argentina.
authors.forename: Diego C
authors.initials: DC
authors.lastname: Fernandez
authors.forename: Laura A
authors.initials: LA
authors.lastname: Pasquini
authors.forename: Damián
authors.initials: D
authors.lastname: Dorfman
authors.forename: Hernán J
authors.initials: HJ
authors.lastname: Aldana Marcos
authors.forename: Ruth E
authors.initials: RE
authors.lastname: Rosenstein
mesh_terms: D000818:Animals; D001253:Astrocytes / Q000378:metabolism; D001369:Axons / Q000648:ultrastructure; D001692:Biological Transport; D001786:Blood Glucose; D001835:Body Weight; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism / Q000473:pathology; D003930:Diabetic Retinopathy / Q000378:metabolism / Q000473:pathology* / Q000517:prevention & control; D004789:Enzyme Activation; D005974:Glutamate-Ammonia Ligase; D019194:Ischemic Preconditioning; D008297:Male; D009836:Oligodendroglia / Q000378:metabolism; D009900:Optic Nerve / Q000098:blood supply* / Q000473:pathology*; D051381:Rats; D012160:Retina / Q000378:metabolism; D012165:Retinal Ganglion Cells / Q000473:pathology*; D013477:Superior Colliculi / Q000378:metabolism; D013997:Time Factors; D050819:Transcription Factor Brn-3A / Q000378:metabolism; D014795:Visual Pathways / Q000098:blood supply* / Q000473:pathology*
chemical_list: D001786:Blood Glucose; D050819:Transcription Factor Brn-3A; D005974:Glutamate-Ammonia Ligase