S-Opsin Contributes to Violet Light-Dependent Refractive Development and Is Associated With Corneal Structural...

To determine whether S-opsin is involved in the refractive response to violet light (VL) in mice and whether loss of Opn1sw is accompanied by corneal structural and biomechanical changes.

Wild-type (WT) and Opn1sw-/- mice were exposed to VL or white light (WL) from 4 to 8 weeks of age. Refractive error, axial length, corneal curvature, and the ratio of axial length to corneal radius (AL/CR) were measured. Retinal morphology and opsin expression were assessed by histological and molecular analyses, and retinal function was evaluated by electroretinography. Corneal biomechanics and extracellular matrix composition were evaluated by atomic force microscopy and molecular analyses.

VL induced a hyperopic shift in WT mice compared with WL (11.83 ± 1.13 D vs. 9.25 ± 0.82 D; P < 0.01) and reduced the AL/CR ratio (2.075 ± 0.030 vs. 2.140 ± 0.021; P < 0.01), without significant changes in AL or CR. At baseline, Opn1sw-/- mice were more myopic than WT littermates (7.00 ± 1.27 D vs. 11.08 ± 0.80 D; P < 0.0001), with a smaller CR (1.395 ± 0.044 mm vs. 1.454 ± 0.021 mm; P < 0.05) and a higher AL/CR ratio (2.240 ± 0.032 vs. 2.156 ± 0.021; P < 0.001). After light exposure, Opn1sw-/- mice failed to exhibit the VL-induced hyperopic response observed in WT mice. Opn1sw deficiency was also associated with reduced photopic electroretinogram (ERG) responses, modest outer nuclear layer thinning, reduced corneal stiffness, and decreased corneal COL4A1 expression.

S-opsin contributes to the refractive response to VL in mice. Loss of Opn1sw is associated with altered corneal curvature, reduced corneal stiffness, and extracellular matrix remodeling in the absence of axial elongation.