Abstract
In the present study, we aimed at better understanding the short (acute) and long term (chronic) degenerative processes characterizing the juvenile rat model of light-induced retinopathy. Electroretinograms, visual evoked potentials (VEP), retinal histology and western blots were obtained from juvenile albino Sprague-Dawley rats at preselected postnatal ages (from P30 to P400) following exposure to 10,000 lux from P14 to P28. Our results show that while immediately following the cessation of exposure, photoreceptor degeneration was concentrated within a well delineated area of the superior retina (i.e. the photoreceptor hole), with time, this hole continued to expand to form an almost photoreceptor-free region covering most of superior-inferior axis. By the end of the first year of life, only few photoreceptors remained in the far periphery of the superior hemiretina. Interestingly, despite a significant impairment of the outer retinal function, the retinal output (VEP) was maintained in the early phase of this retinopathy. Our findings thus suggest that postnatal exposure to a bright luminous environment triggers a degenerative process that continues to impair the retinal structure and function (mostly at the photoreceptor level) long after the cessation of the exposure regimen (more than 1 year documented herein). Given the slow degenerative process triggered following postnatal bright light exposure, we believe that our model represents an attractive alternative (to other more genetic models) to study the pathophysiology of photoreceptor-induced retinal degeneration as well as therapeutic strategies to counteract it.
Highlights
Chronic exposure to bright light is often considered a potential risk factor for the development and the progression of some human retinal diseases, such as Retinitis Pigmentosa (RP) and Age-related Macular Degeneration (AMD) [1,2,3,4]
We have decided to limit our investigation to CNTF only for the following reasons: 1- CNTF was previously shown to be preferentially expressed in the outer segments of the photoreceptors [25], 2- We have previously shown that in the rds mouse model, an intraocular gene transfer of CNTF successfully slowed down the progression of the retinal degeneration and enhanced the retinal function as measured with the ERG [26], and 3Clinical trials are recognizing the efficacy CNTF supplementation in patients affected with Retinitis Pigmentosa and Age-related Macular Degeneration, human retinopathies that are believed to share several features with the animal model of Light-Induced Retinopathy (LIR) [27,28,29,30]
The resulting hemiretinal asymmetry, which is the hallmark of the rodent LIR, could be documented functionally with the Multifocal ERG (mfERG) (Fig 5)
Summary
Chronic exposure to bright light is often considered a potential risk factor for the development and the progression of some human retinal diseases, such as Retinitis Pigmentosa (RP) and Age-related Macular Degeneration (AMD) [1,2,3,4]. One key feature of the LIR model resides in the asymmetric distribution of the resulting light-induced damage, where the superior-temporal quadrant is the retinal region that always shows the most destruction following bright light exposure [5,6,7,9,10]. It is not yet well understood how these hemiretinal differences develop and progress following a bright light insult
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
