April 2009
Volume 50, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2009
Shining Some Light on the Oxygen-Induced Retinopathy (OIR) of Long-Evans (LE) Rats
Author Affiliations & Notes
  • J. Garfinkle
    Ophthalmology/Neurology-Neurosurgery, McGill University-Montreal Children's Hospital, Montreal, Quebec, Canada
  • A. Polosa
    Ophthalmology/Neurology-Neurosurgery, McGill University-Montreal Children's Hospital, Montreal, Quebec, Canada
  • W. Liu
    Ophthalmology/Neurology-Neurosurgery, McGill University-Montreal Children's Hospital, Montreal, Quebec, Canada
  • S. Chemtob
    Ophthalmology/Neurology-Neurosurgery, McGill University-Montreal Children's Hospital, Montreal, Quebec, Canada
  • P. Lachapelle
    Ophthalmology/Neurology-Neurosurgery, McGill University-Montreal Children's Hospital, Montreal, Quebec, Canada
  • Footnotes
    Commercial Relationships  J. Garfinkle, None; A. Polosa, None; W. Liu, None; S. Chemtob, None; P. Lachapelle, None.
  • Footnotes
    Support  Supported by CIHR and Réseau Vision.
Investigative Ophthalmology & Visual Science April 2009, Vol.50, 3607. doi:
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    • Get Citation

      J. Garfinkle, A. Polosa, W. Liu, S. Chemtob, P. Lachapelle; Shining Some Light on the Oxygen-Induced Retinopathy (OIR) of Long-Evans (LE) Rats. Invest. Ophthalmol. Vis. Sci. 2009;50(13):3607.

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

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Abstract

Purpose: : In juvenile albino Sprague-Dawley (SD) and pigmented Long-Evans (LE) rats, postnatal hyperoxia causes a severe retinopathy known as Oxygen Induced Retinopathy (OIR). In contrast, while SD rats show a severe retinopathy following post-eye-opening exposure to bright light (Light-Induced Retinopathy: LIR), the LE retina appears to benefit from such treatment. We examined whether the LIR of the LE rat could mitigate the functional and structural sequelae associated with OIR.

Methods: : Juvenile LE rats were exposed to 80% oxygen and bright cyclic light (10,000 lux; 12D: 12L) between postnatal day (P)6 and P14 (eye opening); P14-P20; and P14-P28. n=14 for each group. Scotopic (intensity: -6.3 to 0.9 log cd.m-2.sec) and photopic (intensity: 0.9 log cd.m-2.sec; background: 30 cd.m-2) flash electroretinograms (fERGs) were recorded at P30 and P60. After each ERG session, rats were euthanized and their eyes collected for histology. Measurements of retinal thickness were then taken.

Results: : The mixed scotopic a-wave, b-wave and Vmax and photopic b-wave amplitudes were significantly reduced at both P30 (to 68%, 22%, 0% and 19% of control respectively) and P60 (to 41%, 15%, 6% and 15% of control respectively) in the P6-P14 group. The P14-20 and P14-28 groups did not demonstrate any significant fERG anomalies at P30, with all fERG parameters at least 85% of control. At P60, however, the scotopic a-wave and b-wave amplitudes were both significantly reduced to 62% of control in P14-P20 while the scotopic a-wave, b-wave and photopic b-wave amplitudes were significantly reduced to 61%, 63% and 70% of control respectively in P14-P28. While exposure from P6-P14 obliterated the outer plexiform layer (OPL) at both P30 and P60, in P14-P28, a significantly thinner OPL (40% of control) was only observed at P60.

Conclusions: : Given the previously demonstrated absence of LIR in rats exposed prior to eye opening, it is not surprising that bright light did not attenuate OIR in the P6-P14 group. Conversely, the P14-P28 group presented with 17% and 30% less functional damage (with respect to scotopic a-wave and Vmax) than rats exposed only to hyperoxia at P30. However, the development of significant functional and structural anomalies in P14-P28 (similar in extent to the hyperoxia-only group) suggests that the beneficial effect of light on OIR is transient. One wonders if the previously demonstrated light-induced upregulation of neurotrophic factors may be responsible for this protective effect.

Keywords: electroretinography: non-clinical • oxidation/oxidative or free radical damage • radiation damage: light/UV 
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