June 2015
Volume 56, Issue 7
Free
ARVO Annual Meeting Abstract  |   June 2015
Enriched environment protects from axoglial alterations of the optic pathway induced by experimental diabetes in adult rats
Author Affiliations & Notes
  • Damian Dorfman
    Human Biochem/Sch of Med, University of Buenos Aires, Buenos Aires, Argentina
  • Marcos Luis Aranda
    Human Biochem/Sch of Med, University of Buenos Aires, Buenos Aires, Argentina
  • Maria Florencia Gonzalez Fleitas
    Human Biochem/Sch of Med, University of Buenos Aires, Buenos Aires, Argentina
  • Pablo Sande
    Human Biochem/Sch of Med, University of Buenos Aires, Buenos Aires, Argentina
  • Ruth Estela Rosenstein
    Human Biochem/Sch of Med, University of Buenos Aires, Buenos Aires, Argentina
  • Footnotes
    Commercial Relationships Damian Dorfman, None; Marcos Luis Aranda, None; Maria Gonzalez Fleitas, None; Pablo Sande, None; Ruth Rosenstein, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2015, Vol.56, 4287. doi:https://doi.org/
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      Damian Dorfman, Marcos Luis Aranda, Maria Florencia Gonzalez Fleitas, Pablo Sande, Ruth Estela Rosenstein; Enriched environment protects from axoglial alterations of the optic pathway induced by experimental diabetes in adult rats. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):4287. doi: https://doi.org/.

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      © ARVO (1962-2015); The Authors (2016-present)

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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 enriched environment (EE) can protect neurons against ischemic damage and diabetic retinopahy, there is no information on its ability to protect axons. We analyzed the effect of enriched environment 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. EE consisted in big cages housing 6 animals and containing several food hoppers, wheels and different objects repositioned once/day and fully substituted once/week starting 3 days after streptozotocin injection. After 6 weeks of diabetes induction, the effect of EE was evaluated using different morphological techniques.

Results: The exposure to EE prevented the deficit in the anterograde transport of CTB from the retina to the superior colliculus, as well as the increase in astrocyte reactivity and microglial activation, axonal neurofilament alterations, decrease in the number of axons, and ultraestructural myelin alterations in the optic nerve distal portion induced by streptozotocin injection.

Conclusions: These results suggest that early vision loss in diabetes could be abated by EE which preserved axonal function and structure.

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