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A. Polosa, W. Liu, S. Chemtob, P. Lachapelle; What Causes the Hemiretinal Disparity in the Light-Induced Retinopathy (LIR) Model?. Invest. Ophthalmol. Vis. Sci. 2009;50(13):3613.
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© ARVO (1962-2015); The Authors (2016-present)
Adult albino rats exposed to a bright luminous environment will promptly develop an asymmetric LIR, where the superior hemiretina (SR) shows more pathology than the inferior one (IR). Juvenile rats will not readily demonstrate this asymmetry. We investigated the dynamic of the pathophysiological processes triggered within the two hemiretinas of the younger rats that ultimately develops into the typical asymmetric retinopathy as the animal ages.
Multifocal ERGs (mfERG: VERIS 5.1; camera display unit, 37 hexagons; white: 200 cd.m-2; black: 0 cd.m-2; background: 100 cd.m-2; bandwidth: 10-100 Hz; N=16) and histology (to determine the thickness of Outer Nuclear Layer (ONL) were performed from P30 throughout P60 (at 5 day intervals) in control and exposed (P14-P28; 12D: 12L; 10 000 lux) juvenile Sprague Dawley rats (N=42). Western blots (N=7) were also carried out in order to compare the levels of CNTF between the two hemiretinas.
Control rats showed no significant hemiretinal disparity, irrespective of age (mean SR/IR ONL thickness ratio: 0.96±0.08). The thickness of the SR ONL was 50%, 26% and 17% of control (p<.05) at P30, P40 and P60 respectively compared to 64%, 53% and 27% (p<.05) for the IR ONL. Significant hemiretinal ONL differences were first seen at P40 (0.53±0.13; p<.05) and remained so until the end of the experiment (P60: 0.54±0.14; p<.05). In control rats, the mfERG SR/IR ratio was 0.95±0.18 compared to 1.91±0.65 (p<.05) for the exposed rats at P30 and 0.65±0.22 (p<.05) and 0.70±0.13 (p<.05) at P40 and P60 respectively. In control rats, western blots revealed a higher basal level of CNTF in the inferior retina (SR/IR ratio: 0.73±0.29). In exposed rats, a transient 15% increase (p<.05) in the SR CNTF level occurred between P35-P40 and returned to basal levels by P45.
While at the onset of the LIR pathophysiological process, the structure and function of the SR and IR are equally affected, that of the SR deteriorates more rapidly in spite of a transient (and probably too late) burst in CNTF activity. We believe that our demonstration of significantly higher CNTF levels in the normal IR could partly explain the hemiretinal discrepancy that characterizes LIR. Finally, one wonder if the enhanced SR function measured at P30 might not reflect the increasing CNTF activity triggered by the light exposure.
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