Optical mechanisms regulating emmetropisation and refractive errors: evidence from animal models

Abstract

Our current understanding of emmetropisation and myopia development has evolved from decades of work in various animal models, including chicks, non‐human primates, tree shrews, guinea pigs, and mice. Extensive research on optical, biochemical, and environmental mechanisms contributing to refractive error development in animal models has provided insights into eye growth in humans. Importantly, animal models have taught us that eye growth is locally controlled within the eye, and can be influenced by the visual environment. This review will focus on information gained from animal studies regarding the role of optical mechanisms in guiding eye growth, and how these investigations have inspired studies in humans. We will first discuss how researchers came to understand that emmetropisation is guided by visual feedback, and how this can be manipulated by form‐deprivation and lens‐induced defocus to induce refractive errors in animal models. We will then discuss various aspects of accommodation that have been implicated in refractive error development, including accommodative microfluctuations and accommodative lag. Next, the impact of higher order aberrations and peripheral defocus will be discussed. Lastly, recent evidence suggesting that the spectral and temporal properties of light influence eye growth, and how this might be leveraged to treat myopia in children, will be presented. Taken together, these findings from animal models have significantly advanced our knowledge about the optical mechanisms contributing to eye growth in humans, and will continue to contribute to the development of novel and effective treatment options for slowing myopia progression in children.

Electroretinogram responses in myopia: a review

“…Several animal species including chicks [35][36][37][38][39][40][41][42][43][44], squid [45], tree shrews [33,46], monkeys [47][48][49][50][51][52][53][54][55], marmosets [56], guinea pigs [57], kittens [58][59][60], mice [61][62][63], and also humans [64][65][66][67][68] are capable of identifying the sign and magnitude of retinal image defocus and make compensatory alterations in ocular growth [69][70][71][72][73][74]. Evidence from the experiments conducted on animal models indicates that the absence of input from the accommodative system (cycloplegia, ciliary nerve section, or damage to the Edinger-Westphal nucleus) [31,39] or higher visual center (optic nerve section) [75] does not influence the ocular response to imposed form-deprivation [38,75], or opt...…”

Tyr is Responsible for the Cctq1a QTL and Links Developmental Environment to Central Corneal Thickness Determination

“…1) Corneal development might be a component of refractive development. Emmetropization typically occurs in the first months following eyelid opening, with impacts from both the amount of light and its focus on the retina 33,38 . Thus, it is feasible that albinism could in effect cause blur (from light not being absorbed by melanin and reflecting within the eye), which induces relative myopia and CCT thinning with rearing in normal lights, but not in dark-rearing.…”

The Correlations between Horizontal and Vertical Peripheral Refractions and Human Eye Shape Using Magnetic Resonance Imaging in Highly Myopic Eyes

“…Thus, the eye can alter the rate of vitreous chamber elongation to restore emmetropia. Visual signals that accelerate axial growth were mediated by mechanisms that operate in a local and regionally selective manner [19]. Peripheral refraction stimulates the elongation of the eye may be due to the fact that the defocus signal is stronger in the peripheral retina than in its center.…”