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E. K. Zimak, A. Polosa, J. Racine, S. Joly, A. L. Dorfman, S. Chemtob, P. Lachapelle; Irreversible Increases in ERG Amplitude and Retinal Thickness Following Postnatal Exposure of Long Evans Rats to Bright Light. Invest. Ophthalmol. Vis. Sci. 2007;48(13):5070.
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In a previous study, we showed that compared to neonatal albino Sprague Dawley (SD) rats, retinal structure and function of pigmented Long Evans (LE) rats were significantly more damaged following postnatal hyperoxia, a finding that we attributed to the suggested pro-oxidant effect of melanin. The purpose of the present study was to further investigate the role of melanin with the use of another oxidative stress namely, bright light.
Scotopic (intensity: -6.3 to 0.6 log cd.sec.m-2; 12 hrs dark adaptation) and photopic (intensity: 0.9 log cd.m-2.sec; background: 30 cd.m-2) ERGs were recorded at P60 from juvenile SD (n=17) and LE (n=8) rats that had been exposed to a bright cyclic light (12D: 12L; 10 000 lux) from P14 to P28. Retinal histology was also performed at P60.
In SD rats, bright light exposure produced a significant decrease (ρ<0.05) in amplitudes of all ERG parameters: rod Vmax (32%), rod-cone a-wave (69%), rod-cone b-wave (34%) and cone b-wave (29%) compared to controls. Similarly, retinal histology revealed a significant (ρ<0.05) decrease in thickness of the photoreceptor layer (PL: 49%), the outer nuclear layer (ONL: 56%) and the outer plexiform layer (OPL: 65%) while the thickness of the inner nuclear layer increased significantly (INL: 72%). In contrast, LE rats showed a significant increase (ρ<0.05) in all ERG parameters (rod Vmax: 42%; rod-cone a-wave: 90%; rod-cone b-wave: 115% and cone b-wave: 145%) compared to normal. Similarly, retinal histology also revealed significant (ρ<0.05) increases in thickness (ONL: 15%; INL: 15% and IPL: 10%) along with a reduction of the PL (41%) and OPL (29%).
Clearly, the above differences between LE and SD cannot be solely attributed to the role of melanin, that is of course unless its role changes (pro-oxidant or free radical scavenger) with the source of free radicals and/or the proximity between the melanin pigment and the cellular target of reactive oxygen species produced by the oxidant. Alternatively one could also postulate that bright light exposure triggered (in LE but not in SD) a significant upregulation of retinal neurotrophic factors that prevented the normal apoptosis process thus explaining the increased retinal thickness and ERG amplitude. The latter hypothesis remains however to be tested.
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