March 2012
Volume 53, Issue 14
Free
ARVO Annual Meeting Abstract  |   March 2012
Exposure To An Enriched Environment As A Novel Strategy To Prevent Acute Ischemic Damage Of The Visual Pathway In Adult Rats
Author Affiliations & Notes
  • Damian Dorfman
    Human Biochem/Sch of Med, University of Buenos Aires, Buenos Aires, Argentina
  • Diego C. Fernandez
    Human Biochem/Sch of Med, University of Buenos Aires, Buenos Aires, Argentina
  • Ruth E. Rosenstein
    Human Biochem/Sch of Med, University of Buenos Aires, Buenos Aires, Argentina
  • Footnotes
    Commercial Relationships  Damian Dorfman, None; Diego C. Fernandez, None; Ruth E. Rosenstein, None
  • Footnotes
    Support  Prestamo BID convocatoria 2006 PICT 1623
Investigative Ophthalmology & Visual Science March 2012, Vol.53, 3477. doi:
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      Damian Dorfman, Diego C. Fernandez, Ruth E. Rosenstein; Exposure To An Enriched Environment As A Novel Strategy To Prevent Acute Ischemic Damage Of The Visual Pathway In Adult Rats. Invest. Ophthalmol. Vis. Sci. 2012;53(14):3477.

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

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Abstract

Purpose: : Ischemia is a key component of several retinal diseases that are leading causes of irreversible blindness. At present, there are no effective strategies to prevent or reverse retinal ischemic damage. Recent evidences indicate that the exposure to an enriched environment (EE) affects the functioning of the visual system. The EE constitutes a strategy that boosts exploratory, visual, and cognitive activities as well as social interaction and voluntary physical exercise. In this context, the aim of the present work was to analyze the effect of exposure to an EE in an acute retinal ischemia model.

Methods: : Adult male Wistar rats were exposed to a standard environment (SE) or EE 3 weeks before and 2 weeks after retinal ischemia. EE consisted of big cages housing 6 animals and containing several food hoppers, wheels and different objects repositioned once/day and fully substituted once/week. Retinal ischemia was induced by increasing intraocular pressure to 120 mm Hg for 40 min. Retinal function (electroretinography, ERG), and histology were analyzed at 7 and 14 days post-ischemia. Anterograde transport from the retina to the superior colliculus (SC) was examined after an intravitreal injection of cholera toxin β-subunit, and retinal and SC glial fibrillary acidic protein (GFAP) levels were assessed by immunohistochemistry.

Results: : In control animals, ischemia induced a significant decrease in ERG a- and b- wave amplitude, whereas the exposure to EE reduced these alterations. In animals exposed to SE, ischemia provoked retinal ganglion cell (RCG) loss which was decreased by exposure to EE. Moreover, ischemia induced a significant increase in GFAP levels in the retina and the SC, and a deficit in the anterograde transport which were reduced in animals exposed to EE.

Conclusions: : These results suggest that the exposure to an EE could become a new strategy for retinal ischemia treatment.

Keywords: neuroprotection • ischemia • electroretinography: non-clinical 
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