Optical correction of induced axial myopia in the tree shrew: implications for emmetropization

Abstract

Purpose: To determine whether an active emmetropization mechanism is involved in the recovery from axial myopia through the use of a mammalian model of refractive development. Specifically, we sought to establish whether the emmetropization mechanism is visually guided by the level of clarity of the image falling on the retina, or if recovery is driven by a mechanism sensitive to abnormal eye shape.

Methods: Young tree shrews had axial myopia induced by monocular deprivation (MD) of pattern vision and then the myopic eye was either: (1) accurately corrected with a negative lens or (2) had a zero-powered lens placed in front of it. Their emmetropization response was monitored, both through the use of ocular refractive and biometric measures, as well as through the assessment of scleral dry weight and glycosaminoglycan synthesis, as indicators of scleral metabolism.

Results: Corrective lenses prevented recovery from induced myopia (-6.8 +/- 0.7 D after 5 days MD vs. -6.6 +/- 0.6 D after 5 days of lens wear), whereas animals fitted with zero-powered lenses displayed near full recovery from the induced myopia (-6.6 +/- 0.6 D vs. -1.7 +/- 0.3 D). Significant reductions in scleral dry weight (-4.6 +/- 1.3%) and glycosaminoglycan synthesis (-28.6 +/- 7.3%) were found in the posterior sclera of animals wearing corrective lenses. Conversely, animals wearing zero-powered lenses displayed elevated levels of glycosaminoglycan synthesis (+62.3 +/- 11.1%) in conjunction with scleral dry weights that did not differ significantly between treated and fellow control eyes (-1.5 +/- 2.6%).

Conclusions: Accurate correction of induced axial myopia prevents the refractive, biometric and scleral metabolic responses that are normally observed in tree shrew eyes recovering from induced myopia. These findings support the hypothesis that recovery is driven by an active emmetropization response dependent on the clarity of image falling on the retina and not by a mechanism that is sensitive to abnormal eye shape.