Purchase this article with an account.
Nicolas Suter, Anna Polosa, Biagio Campanaro, Jonas Galli, Allison L. Dorfman, Pierre Lachapelle; Light Induced Retinopathy in Rats: More Light Same Retinopathy. Invest. Ophthalmol. Vis. Sci. 2011;52(14):1353.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
Bright light exposure causes severe and irreversible damage to retinal structure and function, a condition known as Light Induced Retinopathy (LIR). We examined if LIR characteristics were intensity dependent.
Adult pigmented (Long Evans: LE) and albino (Sprague Dawley: SD) rats were exposed to a cyclic (12L/12D) bright light environment [10 000 lux, n=6 LE and 3 SD; 5000 lux, n=9 LE and 3 SD] for 3 consecutive days. Flash ERGs (fERG: scotopic: -6.3 to 0.6 log cd.sec.m-2 and photopic: 0.9 log cd.sec.m-2; background: 30 cd.m-2) were recorded at 1 day (D1), 15 days (D15) and 30 days (D30) following the cessation of light exposure. The retinas were then collected for histology.
LE RATS: At D1, there was an average 50% reduction (p<.05) in all fERG parameters following the 5000 lux exposure that was not further aggravated (p>.05) following the 10,000 lux exposure or with time. The ONL of the superior retina was 20% of normal thickness following the 5000 lux exposure and completely abolished after the 10000 lux exposure. The inferior ONL was not damaged by either exposure. SD RATS: At D1 there was a significant (p<.05) 81% reduction in all of the fERG components following the 5000 lux exposure that progressed to near extinction after the 10,000 lux exposure and with time. The 5000 lux exposure yielded a severe 70% thinning of the ONL (p<.05 compared to normal) of both retinal hemispheres that was further aggravated to near complete destruction (95% thinning) following the 10,000 lux exposure.
While in SD rats, exposure to a brighter environment will cause a more severe LIR, it does not do so in pigmented LE rats, as if a saturation effect has been reached. These results once again point to inherent differences between photoreceptor cells that make some more resistant and others more labile to environmental stresses. Further elucidation into the mechanisms behind this differential susceptibility will be instrumental in suggesting new therapeutic avenues for some human retinopathies. Funded by the Réseau Vision of the FRSQ and NSERC.
This PDF is available to Subscribers Only