Intrinsic ocular mechanisms underlie lens-induced astigmatism in chicks

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.