March 2012
Volume 53, Issue 14
Free
ARVO Annual Meeting Abstract  |   March 2012
Can Environmental Enrichment (EE) Prevent the Rodent Light-Induced Retinopathy (LIR)?
Author Affiliations & Notes
  • Yasmin Kerouch
    Ophthalmology and Neurology-Neurosurgery, McGill University-Montreal Children's Hospital Research Institute, Montreal, Quebec, Canada
  • Kristina Rousseau
    Ophthalmology and Neurology-Neurosurgery, McGill University-Montreal Children's Hospital Research Institute, Montreal, Quebec, Canada
  • Mathieu Gauvin
    Ophthalmology and Neurology-Neurosurgery, McGill University-Montreal Children's Hospital Research Institute, Montreal, Quebec, Canada
  • Mohammad Quaddoumi
    Department of Applied Therapeutics, Kuwait University, Faculty of Pharmacy, Kuwait
  • Anna Polosa
    Ophthalmology and Neurology-Neurosurgery, McGill University-Montreal Children's Hospital Research Institute, Montreal, Quebec, Canada
  • Pierre Lachapelle
    Ophthalmology and Neurology-Neurosurgery, McGill University-Montreal Children's Hospital Research Institute, Montreal, Quebec, Canada
  • Footnotes
    Commercial Relationships  Yasmin Kerouch, None; Kristina Rousseau, None; Mathieu Gauvin, None; Mohammad Quaddoumi, None; Anna Polosa, None; Pierre Lachapelle, None
  • Footnotes
    Support  FRSQ and Réseau Vision
Investigative Ophthalmology & Visual Science March 2012, Vol.53, 6485. doi:
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      Yasmin Kerouch, Kristina Rousseau, Mathieu Gauvin, Mohammad Quaddoumi, Anna Polosa, Pierre Lachapelle; Can Environmental Enrichment (EE) Prevent the Rodent Light-Induced Retinopathy (LIR)?. Invest. Ophthalmol. Vis. Sci. 2012;53(14):6485.

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

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Abstract

Purpose: : Environmental enrichment (EE) is claimed to reduce several pathogenic mechanisms that are thought to promote retinal degenerative disorders, such as age-related macular degeneration (AMD), presumably by augmenting retinal levels of Brain Derived Neurotrophic Factor (BDNF), a neurotrophin implicated in the neuroprotection of retinal cells. We investigated if prior EE exposure could protect the retinal structure and function in our rodent model of LIR.

Methods: : Adult female Sprague-Dawley rats were group housed (n=9) in an EE consisting of a variety of toys, tubes, nesting material and running wheels in a large mesh cage. Age-matched control rats (CR: n=4) were simultaneously raised in the normal animal care facility (standard environment). After three consecutive weeks of EE, animals were exposed to bright cyclic light of 1500 lux for 3 days to induce the LIR, and then returned to their respective environment for one week. (ERGs) were recorded to measure the efficiency of EE before rearing the animals in the EE (w0) and subsequently (w2 and w3) and 1 (D1) and 7 days (D7) post-LIR.

Results: : At w2 (during EE exposure), the EE group showed reduced scotopic a- and b-wave amplitudes (-23.4% and -28.4% respectively) compared to CR group. At D1 (following light exposure), there was an equal 34% reduction of the scotopic a-wave and 22% of scotopic b-wave amplitudes in both groups. Of interest, while in the CR group the a-wave increased by more than 34% between D1 and D7, in EE rats, it increased by less than 9% (p<.05). During the same time interval, the scotopic b-wave increased by 20% in the CR group while it was significantly reduced by 12% in the EE group.

Conclusions: : EE did not prevent or reduce the pathogenesis of LIR. If anything it would appear to have exacerbated it. Furthermore, even before inducing the LIR, EE had already hampered retinal function. One wonders if the 3 week EE exposure could not have introduced an additional stress factor that could have enhanced neuronal vulnerability to ensuing light-induced excitotoxicity.

Keywords: retinal degenerations: cell biology • neuroprotection • age-related macular degeneration 
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