September 2016
Volume 57, Issue 12
Open Access
ARVO Annual Meeting Abstract  |   September 2016
Intrinsic Ocular Mechanisms Underlie Lens-Induced Astigmatism in Chicks
Author Affiliations & Notes
  • William K Stell
    Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada
  • Vanessa Popa
    Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada
  • Chea-Su Kee
    School of Optometry, The Hong Kong Polytechnic University, Kowloon, Hong Kong
  • Footnotes
    Commercial Relationships   William Stell, None; Vanessa Popa, None; Chea-Su Kee, None
  • Footnotes
    Support  NSERC Grant RGPIN 131-2013; UGC-GRF PolyU 151011/14M
Investigative Ophthalmology & Visual Science September 2016, Vol.57, No Pagination Specified. doi:
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      William K Stell, Vanessa Popa, Chea-Su Kee; Intrinsic Ocular Mechanisms Underlie Lens-Induced Astigmatism in Chicks. Invest. Ophthalmol. Vis. Sci. 201657(12):.

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      © 2017 Association for Research in Vision and Ophthalmology.

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Abstract

Purpose : Ocular astigmatism is a refractive error due to differential meridional powers of ocular components, causing blurred vision at all viewing distances. The cause(s) remain poorly understood. Here we used a novel animal model of lens-induced astigmatism to test the hypothesis that processing of astigmatic images in retinal circuits causes the optical abnormality

Methods : We induced astigmatism by mounting +4.00/-8.00D crossed-cylinder lenses over the right (treated) eyes of 7-day-old chicks (P7), in groups of n=12, with the -8.00D axis oriented vertically (at 90°) or horizontally (180°); the left (fellow) eyes wore no lens. Net refractive errors of both eyes were measured by streak retinoscopy, before and after 1 week of lens-wear; in selected cases the corneal component was measured by keratometry. To test whether neuronal pathways between retina and brain are required, we injected tetrodotoxin (TTX; 7µL of 10-4M) or PBS (7µL) into the vitreous of the treated eyes on P7, P9 and P11; we assessed the efficacy and duration of action of TTX by the pupillary light reflex and optokinetic response (n=6 each). To confirm that retinal circuitry is required, we injected mixed excitotoxins (2µmol N-methyl-D-aspartate, 0.2µmol quisqualic acid, 0.2µmol kainic acid; in 20µL water) into the treated eyes of n=12 chicks at P7. Fellow eyes always received vehicle alone. Interocular differences (treated - fellow) were assessed by 2-tailed unpaired t-test, or 2-way ANOVA + Tukey’s post-test.

Results : Crossed-cylinder goggles reliably induced refractive astigmatism. Maximum astigmatic error was induced at 90°, by -8.00DC axis oriented vertically; this compensated for the imposed defocus. Treated eyes developed astigmatism after injecting TTX or PBS, but not after excitotoxins. Keratometry confirmed that the cornea itself was astigmatic.

Conclusions : In our chicks, crossed-cylinder lenses reliably induced compensatory astigmatism. Prevention of astigmatism by excitotoxins showed that the mechanism requires the retina, and not some other light-sensitive ocular tissue (e.g., iris); furthermore, the failure of TTX to affect astigmatism showed that extraretinal neural pathways are not required. We suggest that lens-induced astigmatism is due to local mechanisms of scleral growth-regulation by image defocus, plus mechanical deformation of the cornea by the distorted sclera.

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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