June 2013
Volume 54, Issue 15
Free
ARVO Annual Meeting Abstract  |   June 2013
Extremely brief light-preconditioning in pigmented mouse model of light-induced retinal degeneration (LIRD)
Author Affiliations & Notes
  • Priscila Cunha
    Ophthalmology, Emory University School of Medicine, Atlanta, GA
  • Micah Chrenek
    Ophthalmology, Emory University School of Medicine, Atlanta, GA
  • Jana Sellers
    Ophthalmology, Emory University School of Medicine, Atlanta, GA
  • Jeffrey Boatright
    Ophthalmology, Emory University School of Medicine, Atlanta, GA
  • Footnotes
    Commercial Relationships Priscila Cunha, None; Micah Chrenek, None; Jana Sellers, None; Jeffrey Boatright, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2013, Vol.54, 2011. doi:
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      Priscila Cunha, Micah Chrenek, Jana Sellers, Jeffrey Boatright; Extremely brief light-preconditioning in pigmented mouse model of light-induced retinal degeneration (LIRD). Invest. Ophthalmol. Vis. Sci. 2013;54(15):2011.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose: Preconditioning of albino mice using moderate intensity cyclic light may be confounded due to shortened photoreceptor outer segments and reduced rhodopsin expression such that the retinas are less sensitive to light. We hypothesize that preconditioning can be induced in pigmented mice with brief, sub-toxic light exposure. Here we describe the parameters used to induce such preconditioning.

Methods: Sixty-four male 129sv mice were obtained from Charles River (100 days old) and kept in a 12:12 light: dark cycle. Light-preconditioning was done using the following procedure: mice were treated with 1% atropine eye drops at 9:00AM and maintained in the dark for 1 hour to allow the pupils to dilate. Non-toxic light exposure consisted of 5k lux of white light for four hours using a LED lamp. Light-preconditioning was done either 1 or 3 days before LIRD. LIRD was done according to the following procedure: at 9:00AM mice were treated with 1% atropine eye drops and maintained in the dark for 1 hour to allow the pupils to dilate. Toxic light exposure consisted of 40-50k lux of white light for four hours using a LED lamp. Visual acuity was measured using OptoMetry optokinetic tracking system (OKT). Retinal function was assessed using ERGs: scotopic a- and b-waves were measured using 5 flash intensities (0.0039-24.9 cd s/m^2).

Results: We found that intense white light causes light damage in 129sv mice. This can reliably be measured with either OKT (82% of dim controls, P<0.001) or ERG (43% of dim controls, P=0.01). Preconditioning treatment of 5k lux alone does not cause a diminishment of retinal function either by OKT or ERG. Preconditioning mouse retinas either 1 day or 3 days prior to light damage prevents loss of visual acuity as measured by OKT (97% of dim controls for both, P<0.001 versus non-conditioned bright). Preconditioning mouse retinas 3 days prior to light damage prevents loss of photoreceptor function as measured by ERG (64% of dim controls, P=0.065 versus non-conditioned bright).

Conclusions: In pigmented 129sv mice, treatment with only 4h of non-toxic bright light prevents damage from later exposure to toxic levels of light. Future experiments include examining whether outer segment length and rhodopsin expression are maintained in this approach.

Keywords: 615 neuroprotection • 695 retinal degenerations: cell biology • 688 retina  
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