Does Emmetropization Need Rods?

Because high visual acuity is a function of the fovea and because myopia has severe effects on distance visual acuity, one tends to extrapolate that emmetropization must also be controlled by the fovea. However, while it is clear that the fovea controls accommodation, its role in emmetropization is not so clear. Instead, there is recent evidence that the peripheral retina guides emmetropization, also in foveate animals. ¹ Most mammals, including mice, have more rods than cones (a ratio of 95 rods to 5 cones is typical). ² Cones are clustered in the fovea but their density drops rapidly a few degrees away. Despite their low density, they can provide excellent color and motion vision in the periphery. It remains to the 95% rods to capture the few photons that are available at low luminances, which explains why they need to cover most of the retinal area. But if they are so abundant it is hard to believe that they are excluded from the mechanism of emmetropization. How do their (saturated?) signals contribute to vision and emmetropization when luminance is high? Their low acuity is not necessarily a problem (one does not need high spatial resolution to determine the best focus, it is enough to maximize image contrast). In mice, it was found that mutants with only rods have much better visual acuity than with only cones. Park and colleagues ³ have now tested whether a rod knockout mouse, Gnat1^−/− can emmetropize at all. It was found that they could not (emmetropization is assumed to be functional if animals develop deprivation myopia when diffusers are placed in front of their eyes). At the same time, they had much lower retinal dopamine production, a neurotransmitter known to be important in emmetropization. There are certainly limitations of mouse studies, small effects on refraction, often no significant changes in axial length, long treatment periods necessary, but these findings support the idea that rods play an important role in emmetropization.