Retinal control of lens-induced astigmatism in chicks

Anca-Vanessa Popa; Chea-Su Kee; William K Stell

doi:10.1016/j.exer.2020.108000

Retinal control of lens-induced astigmatism in chicks

Exp Eye Res. 2020 May:194:108000. doi: 10.1016/j.exer.2020.108000. Epub 2020 Apr 9.

Authors

Anca-Vanessa Popa¹, Chea-Su Kee², William K Stell³

Affiliations

¹ O'Brien Centre for the Bachelor of Health Sciences Program, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada.
² School of Optometry, The Hong Kong Polytechnic University, Hong Kong Special Administrative Region; Interdisciplinary Division of Biomedical Engineering, The Hong Kong Polytechnic University, Hong Kong Special Administrative Region.
³ Department of Cell Biology and Anatomy and Department of Surgery, Hotchkiss Brain Institute and Alberta Children's Hospital Research Institute, Cumming School of Medicine, University of Calgary, Calgary, Alberta, T2N 4N1, Canada. Electronic address: wstell@ucalgary.ca.

PMID: 32171734
DOI: 10.1016/j.exer.2020.108000

Abstract

Purpose: Astigmatism is a refractive error due to meridional differences in refractive powers of lens or cornea. The resulting failure to focus image points in a single plane causes blurred vision at all distances. In this study, using an animal model of lens-induced astigmatism, we tested the hypothesis that induced astigmatism is due to processing of astigmatic retinal image information by the brain, which causes distorted growth in the anterior segment via centrifugal neural projections.

Methods: To induce astigmatism, +4.00DS/-8.00DC crossed-cylinder-lens goggles were affixed over the right eyes of 7-day-old chicks (P7), with the -8.00DC axis oriented vertically (at 90°) or horizontally (180°) (n = 12 each); the left eyes were without goggles (non-goggled). For all experiments, refractive errors of both eyes were measured by streak retinoscopy, before and after 1 week of lens wear. To test whether neuronal pathways between retina and brain are required, axonal conduction within the eye was blocked by intravitreal injections of tetrodotoxin (TTX; 7 μL of 10^-⁴M) in phosphate-buffered saline (PBS), or of PBS alone (7 μL); fellow open eyes received PBS alone. Pupillary light reflex (PLR) and optokinetic response (OKR) were measured, to assess the efficacy and duration of TTX action. To test whether retinal circuitry is required, groups of chicks (n = 12 each) were treated at P7 by intravitreal injection of 20 μL of mixed excitotoxins (2 μmol N-methyl-D-aspartate, 0.2 μmol quisqualic acid, 0.2 μmol kainic acid; in water) into goggled or non-goggled eyes, to compromise retinal circuitry needed for emmetropization.

Results: Crossed-cylinder goggles reliably induced refractive astigmatism. Maximum astigmatic error was induced when the cylindrical axis was oriented at 90° (vertically). TTX effectively blocked nerve conduction within the eye for 48 h after injection. Goggled eyes developed astigmatism after treatment with TTX or PBS, but not after excitotoxins.

Conclusion: Our hypothesis was rejected. In this model, the compensatory astigmatism induced by crossed-cylinder lenses is intrinsic to the eye, and mediated by visual processing in the retina.

Keywords: Astigmatism; Chicks; Crossed-cylinder lens; Excitotoxin; Retina; Tetrodotoxin.

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

Accommodation, Ocular / physiology*
Animals
Astigmatism / etiology
Astigmatism / pathology*
Astigmatism / physiopathology
Chickens
Disease Models, Animal
Eyeglasses / adverse effects*
Male
Refraction, Ocular / physiology*
Retina / pathology*
Retinoscopy