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Frank Schaeffel, Carina Kelbsch, Paul Richter, Barbara Wilhelm, Helmut Wilhelm; Melanopsin - does it modulate the susceptibility to myopia?. Invest. Ophthalmol. Vis. Sci. 2016;57(12):2494.
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© 2017 Association for Research in Vision and Ophthalmology.
There is considerable epidemiological and experimental evidence that exposure to bright light has an inhibitory effect on myopia development. Since ambient illuminance is poorly specified by the transient photoreceptor signals, the more tonic responses of ipRGCs (intrinsically photosensitive retinal ganglion cells, using melanopsin as photopigment) may be better candidates. Furthermore, it was recently found (Chakraborty et al, ARVO 2015, #5843) that melanopsin knock-out mice become more myopic during deprivation of sharp vision. We used the difference in the pupil responses to blue and red light to quantify melanopsin signal strength and correlated it to age and refractive errors of the subjects.
A small portable video pupillograph was developed to record pupil responses to 2.9 sec blue (LEDs 460 nm) and red flashes (LEDs 630 nm). It is known that recovery of pupil size after light stimulation in the blue is delayed, compared to the red, due to the contribution of melanopsin. The area between the red and blue flash response curves in the 1.7 sec window after the light went off was taken as a measure of melanopsin contribution, after normalization to baseline pupil area (MI). Twenty-two subjects, with ages ranging from 17 to 87 years, were measured.
MI was highly variable among subjects, and differences between subjects were often highly significant. As found in other studies, pupil size declined with age (0.02 mm per year (R=0.681, p<0.005). A weak invrese correlation was found between MI and age (R=0.441, p<0.05). However, MI was NOT correlated with the refractive errors of the subjects (R=0.328, n.s.).
Despite conspicious inter-individual differences in nMI, there was no obvious correlation to refractive error. The small age effect could be due to yellowing of the lens in older subjects. It could be that our sample was too small, the ages too scattered or that too few subjects were included with higher refractive errors but our study does not support the idea of a role of melanopsin in the development of myopia. To finally clarify this question, the study should be extended to children with progressing myopia and of similar age, who are exposed to similar visual environments.
This is an abstract that was submitted for the 2016 ARVO Annual Meeting, held in Seattle, Wash., May 1-5, 2016.
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