Abstract
To unravel the mechanisms behind the higher resistance to light damage of juvenile (JR) versus adult (AR) rats, Sprague Dawley rats were exposed to a bright luminous environment of 10, 000 lux. The light-induced retinopathy (LIR) was assessed with histology, electroretinography and immunohistochemistry (IHC). In JR, 2 days of exposure induced the typical LIR, while >3 days added little LIR. IHC revealed a subtle migration of microglia (Iba1 marker) from the inner to the outer retina after 3 days of exposure in JR contrasting with the stronger reaction seen after 1 day in AR. Similarly, in JR, the Müller cells expressed less intense GFAP, CNTF and FGF2 staining compared to AR. Our results suggest that in JR the degree of retinal damage is not proportional to the duration of light exposure (i.e., dose-independent retinopathy), contrasting with the dose-dependent LIR reported in AR. The immature immune system in JR may explain the delayed and/or weaker inflammatory response compared to AR, a finding that would also point to the devastating contribution of the immune system in generating the LIR phenotype, a claim also advanced to explain the pathophysiology of other retinal degenerative disorders such as Age-related Macular Degeneration, Diabetic Retinopathy and Retinitis Pigmentosa.
Highlights
Bright light exposure is known to trigger severe and irreversible retinal damage and there is growing evidence linking the pathophysiology of the rodent light-induced retinopathy (LIR) with human retinal disorders such as Retinitis Pigmentosa and Age-related Macular Degeneration [1,2]
Another aim of our study was to determine if age-dependent differences in the immune and cellular responses at the onset of the light exposure could explain the higher intrinsic resistance to light-induced damage found in juvenile rats compared to adult rats
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Summary
Bright light exposure is known to trigger severe and irreversible retinal damage and there is growing evidence linking the pathophysiology of the rodent light-induced retinopathy (LIR) with human retinal disorders such as Retinitis Pigmentosa and Age-related Macular Degeneration [1,2]. Damage in the inferior retina remains relatively uniform (i.e., no significant variations with eccentricity), at least in the early stages of the disease [6], creating distinctive superior-inferior hemiretinal differences which is the hallmark of the LIR model Given that this photoreceptor hole (i.e., in the superior retina) is present immediately following the end of the light exposure, one aim of this study was to determine, in juvenile rats, the minimal duration of light-exposure required to cause the typical hemiretinal difference (i.e., first appearance of the photoreceptor hole in the superior hemiretina only). Another aim of our study was to determine if age-dependent differences in the immune and cellular responses at the onset of the light exposure could explain the higher intrinsic resistance to light-induced damage found in juvenile rats compared to adult rats
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