May 2006
Volume 47, Issue 13
ARVO Annual Meeting Abstract  |   May 2006
Light–Induced Photoreceptor Degeneration in Juvenile Rats: Some Die Others Don't! Why?
Author Affiliations & Notes
  • S. Joly
    University of Montreal, Montreal, PQ, Canada
  • V. Pernet
    University of Montreal, Montreal, PQ, Canada
    Pathology and Cellular Biology,
  • S. Chemtob
    Pharmacology and Therapeutics, McGill University, Montreal, PQ, Canada
  • A. Di Polo
    University of Montreal, Montreal, PQ, Canada
    Pathology and Cellular Biology,
  • P. Lachapelle
    University of Montreal, Montreal, PQ, Canada
    Ophthalmology, McGill University– Montreal Children's Hospital Research Institute, Montreal, PQ, Canada
  • Footnotes
    Commercial Relationships  S. Joly, None; V. Pernet, None; S. Chemtob, None; A. Di Polo, None; P. Lachapelle, None.
  • Footnotes
    Support  Supported by CIHR and Réseau Vision du FRSQ.
Investigative Ophthalmology & Visual Science May 2006, Vol.47, 3083. doi:
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      S. Joly, V. Pernet, S. Chemtob, A. Di Polo, P. Lachapelle; Light–Induced Photoreceptor Degeneration in Juvenile Rats: Some Die Others Don't! Why? . Invest. Ophthalmol. Vis. Sci. 2006;47(13):3083.

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

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Purpose: : We have previously reported that, compared to adults, the retina of juvenile Sprague Dawley (SD) rats possessed a remarkable endogenous resistance to light–induced retinopathy (LIR). The aim of this study was to further explore the cellular and molecular mechanisms at the origin of this neonatal protection.

Methods: : Juvenile SD rats were exposed to a bright luminous environment (10000 lux; 12 hours/day) from P14–P20 or P14–P28. Retinal histology was performed either immediately after the offset of the light exposure or at 2 months of age. Retinal cell death was quantified with the TUNEL method. Protein levels and retinal localization of FGF–2, CNTF and BDNF were determined by western–blots and immunohistochemistry, respectively.

Results: : The kinetic of LIR was different after 6 and 14 days of exposure. Immediately following 6 days of exposure, the ONL was reduced to 64% (P<.05) of control and further reduced to 51% (P<.01) in rats aged 2 months. In contrast, immediately following a 14–day exposure to the same environment, the ONL was reduced to 46% (P<.001) of control, a value that remained unchanged at 2 months. These results correlated with the number of TUNEL–positive cells identified in both groups. Western–blot analysis demonstrated that FGF–2 and CNTF were strongly upregulated in juvenile rats after light exposure, while BDNF protein level was unchanged. FGF–2 and CNTF upregulation occurred in the inner nuclear layer of the retina and co–immunostaining with CRALBP and GFAP revealed that Müller cells expressed both neurotrophic factors. Our data showed that both retinal hemispheres were similarly damaged just after exposure, although the superior retina was the most affected in adult animals. Strikingly, FGF–2 and CNTF protein levels were similar in the superior and the inferior hemisphere.

Conclusions: : Our 6 vs 14–day exposure differences strongly suggest that only half of the juvenile retinal photoreceptors will degenerate (immediately or subsequently) as a result of LIR. An accurate identification of the differences between the more and less susceptible photoreceptors will be instrumental in devising therapeutic strategies. In that respect our data suggests that FGF–2 and CNTF may play a neuroprotective role in the retina after bright light exposure but other mechanisms may to be involved.

Keywords: radiation damage: light/UV • retina • neuroprotection 

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