EARLY CHRONIC MONOCULAR VISUAL DEPRIVATION COMPROMISES THE RETINAL FUNCTION OF THE DEPRIVED EYE

Abstract

Amblyopia is caused by abnormal visual experience during early childhood such as unilateral cataract, strabismus, and anisometropia. The misalignment of the images in the case of strabismus or blurriness/haziness of the image quality originating from the defective eye results in reduced visual acuity and contrast sensitivity in the deprived eye (Volkers et al., 1987) in comparison to the non-deprived eye and limits stereopsis in humans (Husk et al., 2012). Most clinical treatments for amblyopia penalize the fellow eye to bias the visual system towards the input from the amblyopic eye. Unfortunately, current clinical treatments for amblyopia are most effective in children younger than 7 years old (Cotter et al., 2012). Works in animal models of amblyopia are beginning to identify ways to improve vision in adult amblyopes. They have focused almost exclusively on deficits in the functions of the visual cortex. However, dark rearing can reduce the amplitude of the photopic Electroretinogram indicating reduced functions of cone-mediated retinal functions and alter the mGluR6 distribution and intensity in the first synapses between cone photoreceptors and ON bipolar cells (Dunn et al., 2013). It is predicted but not yet tested, that monocular deprivation will have a similar impact on retinal functions. Here we characterize various aspects of the effect of chronic monocular deprivation (cMD) on retinal functions in adult mice. We observed that chronic monocular deprivation significantly reduced electroretinogram (ERG) response originating from the inner retinal plexiform layer of the deprived eye retina in comparison to the non-deprived eye retina. Our observation suggests that early chronic visual deprivation compromises the retinal function of the deprived eye of the adult mice.