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Título:
Ischemic conditioning protects from axoglial alterations of the optic pathway induced by experimental diabetes in rats
Autor/es:
FERNANDEZ DC; DORFMAN D; ROSENSTEIN RE
Lugar:
Seattle
Reunión:
Congreso; The Association For Research In Vision And Ophthalmology (Arvo); 2013
Institución organizadora:
ARVO
Resumen:
Invest Ophthalmol Vis Sci 2013;54: E-Abstract 3245.© 2013 ARVO
3245?A0036
Ischemic conditioning
protects from axoglial alterations of the optic pathway induced by experimental
diabetes in rats
Diego
Fernandez1, Damian Dorfman1 and Ruth Rosenstein1
1 Universidad de
Buenos Aires/CONICET, Buenos Aires, Argentina
Commercial
Relationships: Diego
Fernandez, None; Damian Dorfman, None; Ruth Rosenstein, None
Support: None
Abstract
Purpose: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.
Methods: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.
Results: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.
Conclusions:These results suggest that early
vision loss in diabetes could be abated by ischemic conditioning which
preserved axonal function and structure.
Keywords: 499 diabetic retinopathy ? 540 glia
? 629 optic nerve
©
2013, The Association for Research in Vision and Ophthalmology, Inc., all
rights