Flicker parameters are different for suppression of myopia and hyperopia

Abstract

Axial eye growth rates in the chicken are controlled by local retinal image-processing circuits. These circuits quantify the loss of contrast for different spatial frequencies and promote axial eye growth rates in correlation with the amount of retinal image degradation (“deprivation myopia”). They also distinguish whether the plane of focus lies in front of or behind the retina. How the sign of defocus is detected still remains unclear. Cues from chromatic aberration are not important. In an attempt to isolate retinal circuits controlling the development of myopia or hyperopia, young chickens were raised in flickering light of different frequencies (12 and 6 Hz) and duty cycles (4–75 %) produced by rotating chopper disks. The effects of flickering light on refractive errors and change in axial growth rates induced by translucent occluders or defocusing lenses were measured by infrared retinoscopy and A-scan ultrasound, respectively. Retinal electrical activity was evaluated by flicker ERG after matching flicker parameters and stimulation brightness at retinal surface. Changes in retinal and vitreal dopamine content caused by flicker in occluded and normal eyes were determined by HPLC-ECD. Strikingly, suppression of myopia occurred for similar flicker parameters, whether induced by translucent occluders (“deprivation”) or negative lenses (“defocus”). The degree to which myopia was suppressed was correlated with the duration of flicker dark phase and with the ERG amplitude. In contrast, suppression of hyperopia did not correlate with these parameters. We conclude that two different retinal circuits with different temporal characteristics are involved in the processing of hyperopic defocus/deprivation and of myopic defocus, the first one dependent on flicker ERG amplitude. However, we did not find any correlation between the rate of dopamine release and the degree of inhibition of deprivation myopia in flickering light.