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Giedrius Kalesnykas, Symantas Ragauskas, Simon Kaja, Heikki Tanila, Henri Olavi Leinonen; Age-related differences in light sensitivity in BALB/c mice. Invest. Ophthalmol. Vis. Sci. 2016;57(12):5004.
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© ARVO (1962-2015); The Authors (2016-present)
Exposure of BALB/c mice to bright light is an established preclinical model for the dry form of age-related macular degeneration. Here we tested the hypothesis that aged BALB/c mice show differential functional deficits after light damage compared to young mice.
Two and five months old male BALB/c mice (n=6) were exposed to bright light (10,000 lux) for 14 hours. Age- and gender-matched controls (n=6) were kept under normal light conditions. Retinal function was evaluated on day 1 and on day 7 after exposure to bright light using flash electroretinogram (fERG). Outer nuclear layer (ONL) thickness was measured using in vivo optical coherence tomography (OCT; Envisu R2200 system, Bioptigen Inc., NC, USA). At the end of a 7-day follow-up period, mice were sacrificed and eyes were cryosectioned. Ocular sections were stained for hematoxylin and eosin (H&E), terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) and quantified using microscopy.
Functional measurements of young BALB/c mice showed a 34% decrease in the a-wave amplitude and a 29% decrease in the b-wave amplitude as compared to naïve young mice controls. In contrast, aged BALB/c mice showed a 20% decrease in the a-wave amplitude and a 15% decrease in the b-wave amplitude as compared to naïve aged mice controls. The thickness of the outer nuclear layer (ONL) significantly decreased in the superior temporal quadrant of the eye by 20% in aged mice and by 32% in young mice. Quantitative analysis of TUNEL staining confirmed photoreceptor cell death in ONL.
Young BALB/c mice are more susceptible to functional deficits and morphological retinal damage after exposure to bright light compared with aged old BALB/c mice. Our data provide new evidence for differential regulation of cell death mechanisms during aging and contribute to the understanding of the molecular mechanisms of light damage.
This is an abstract that was submitted for the 2016 ARVO Annual Meeting, held in Seattle, Wash., May 1-5, 2016.
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