Effects of experimental myopia in a novel mouse model of rod dysfunction
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Saminath Gandhi, Ramnath
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Abstract
Myopia is a refractive error caused by excessive axial elongation of the eye and is becoming a major global health concern. Rod photoreceptors have been suggested to play a role in signaling pathways that regulate eye growth, with prior studies indicating they may be required for the development of form-deprivation myopia (FDM). However, these findings may be confounded by the genetic makeup of the model. In this study, we tested the role of rod phototransduction in myopia using a novel Gnat1ex2 mouse model generated with CRISPR on a C57BL/6J background. Form-deprivation and lens-induced myopia (LIM) models were induced at P28 using a frosted diffuser or a −10 D lens. Refractive error, corneal curvature, and axial parameters were measured for 2 weeks, and visual function was assessed using optomotor response. Both FDM and LIM produced significant myopic shifts. However, no differences were observed between Gnat1ex2/ex2 mice and controls in refractive error, corneal curvature, axial parameters, or optomotor responses (OMR). Ocular growth followed normal patterns across all groups. Overall, these results show that functional rod photoreceptors are not required for the development of experimental myopia in this model. This suggests that other retinal pathways may compensate or be responsible for myopic eye growth.
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2026-05
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Text
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Undergraduate Thesis