Light‐Induced Retinopathy in neonatal rats: A new retinal degeneration slow model
Purpose We showed that compared to adult rats (AR), the retina of neonatal rats (NR) is significantly more resistant to light damage. The purpose of this study was to determine the minimum exposure time that the neonatal retina requires to cause an adult‐like retinopathy at long term. Methods Starti...
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Veröffentlicht in: | Acta ophthalmologica (Oxford, England) England), 2015-10, Vol.93 (S255), p.n/a |
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Sprache: | eng |
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Zusammenfassung: | Purpose
We showed that compared to adult rats (AR), the retina of neonatal rats (NR) is significantly more resistant to light damage. The purpose of this study was to determine the minimum exposure time that the neonatal retina requires to cause an adult‐like retinopathy at long term.
Methods
Starting at postnatal age 14 days (P14), NR were exposed to 10,000 lux for various lengths of time [1, 2, 3, 6, 9, 12 and 16 consecutive days (d)]. ERGs and retinal histology were performed at predetermined time points.
Results
Maximal effect was obtained after 3 days of exposure [50% control ONL thickness (p 0.05) thinning of the ONL was observed. In contrast, a significant (p 0.05) to the damage produced following a 14 day long exposure.
Conclusions
Our findings suggest that in NR, a one day long light exposure is sufficient to produce, at long term, a significant retinal degeneration that will significantly impact the retinal structure and function and that in spite of the fact that no measurable structural and functional retinal anomalies could be demonstrated immediately following this 1‐day exposure (i.e. at P15). Our light‐induced slow retinal degeneration model thus represents an attractive (especially its dose‐dependent nature) alternative (to other more genetic models) to study the pathophysiology of photoreceptor‐induced retinal degeneration and therapeutic strategies to counteract it. Funding: CIHR and FRQ‐S, under the frame of E‐Rare‐2, the ERA‐Net for Research on Rare Diseases. |
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ISSN: | 1755-375X 1755-3768 |
DOI: | 10.1111/j.1755-3768.2015.0471 |