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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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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.
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.
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.
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.
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