May 2004
Volume 45, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2004
LIGHT–INDUCED RETINOPATHY: FROM THE NEWBORN TO THE ADULT RATS.
Author Affiliations & Notes
  • S. Joly
    Département de Sciences biologiques,
    Université de Montréal, Montreal, PQ, Canada
  • V. Pernet
    Département de Pathologie et biologie cellulaire,
    Université de Montréal, Montreal, PQ, Canada
  • A. Dorfman
    Pharmacology and Therapeutics, McGill University, Montreal, PQ, Canada
  • A. Di Polo
    Département de Pathologie et biologie cellulaire,
    Université de Montréal, Montreal, PQ, Canada
  • S. Chemtob
    Pharmacology and Therapeutics, McGill University, Montreal, PQ, Canada
  • H. Moukhles
    Département de Sciences biologiques,
    Université de Montréal, Montreal, PQ, Canada
  • P. Lachapelle
    Département de Sciences biologiques,
    Université de Montréal, Montreal, PQ, Canada
    Ophthalmology, McGill University/Montreal Children's Hospital Research Institute, Montreal, PQ, Canada
  • Footnotes
    Commercial Relationships  S. Joly, None; V. Pernet, None; A. Dorfman, None; A. Di Polo, None; S. Chemtob, None; H. Moukhles, None; P. Lachapelle, None.
  • Footnotes
    Support  none
Investigative Ophthalmology & Visual Science May 2004, Vol.45, 1356. doi:
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      S. Joly, V. Pernet, A. Dorfman, A. Di Polo, S. Chemtob, H. Moukhles, P. Lachapelle; LIGHT–INDUCED RETINOPATHY: FROM THE NEWBORN TO THE ADULT RATS. . Invest. Ophthalmol. Vis. Sci. 2004;45(13):1356.

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

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Abstract

Abstract: : Purpose:To characterize the light–induced retinopathy (LIR) from newborn to adulthood in Sprague–Dawley rats. Methods: Female Sprague–Dawley rats with their litters were maintained under bright cyclic light (10000 lux; 12D: 12L) from birth to postnatal day 14 (P0– P14), from P14 to P20 or from P14 to P28. Electroretinograms (ERGs) and retinal histology were obtained at one month of age. Results: After less than 6 days of light exposure, the mother’s ERGs were nearly abolished. In contrast, there was no evidence of LIR in the P0– P14 rats, while the ERGs were significantly attenuated in the P14– P20 (a–wave: 50%; b–wave: 65% of control amplitude; P<0.01) and even more in the P14 P28 group (a–wave: 16%; b–wave: 43% of control amplitude; P<0.01). Histological analysis of the mother’s retinas revealed the complete disappearance of the Outer Nuclear Layer (ONL) and Outer Plexiform Layer (OPL). In contrast, newborn rats exposed from P0– P14 showed little effect on ONL thickness, while exposure from P14– P28 led to a 60% decrease of the ONL thickness. In contrast the OPL was already 68% thinner than normal in P0– P14 group and further attenuated to 29 % of normal in the P14– P28 group. Conclusions: Perinatal exposure to an intense luminous environment does not yield the severe retinopathy observed in adult rats subjected to an identical environmental insult. Our demonstration of the lack of an adult–like retinopathy even at an age when the eyelids are open (P14 P28 group) rules out the protective effect of the eyelids as an explanation for the near absence of an LIR in the P0 P14 group. Our results would thus support the claim of a relative perinatal retinal immunity to environmental toxic stresses previously shown to exist in our oxygen–induced retinopathy model. Funded by CIHR and Réseau Vision.

Keywords: radiation damage: light/UV • electroretinography: non–clinical • retina: distal (photoreceptors, horizontal cells, bipolar cells) 
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