Ashby RS, Schaeffel F.
Institute for Ophthalmic Research, Section of Neurobiology of the Eye, University of Tübingen, Tübingen, Germany. regan.ashby@anu.edu.au
Invest Ophthalmol Vis Sci. 2010 Oct;51(10):5247-53.
This study looked at how bright light affected the development of refractive error (myopia or hyperopia) induced by optical defocus (caused by plus or minus lenses, +7 or -7). The chicks with minus lenses that were exposed to 15, 000 lux (brighter than a SAD lamp, much brighter than typical indoor lux levels) for 5 hours per day developed myopia at a slower rate than those exposed to 500 lux (what one might be exposed to typically indoors). The role of dopamine was found to be important: when the chicks were injected with a dopamine antagonist, the protective effect of the light against myopia was negated.
"It has been shown that sunlight or bright indoor light can inhibit the development of deprivation myopia in chicks. It remains unclear whether light merely acts on deprivation myopia or, more generally, modulates the rate of emmetropization and its set point. This study was conducted to test how bright light interacts with compensation for imposed optical defocus. Furthermore, a dopamine antagonist was applied to test whether the protective effect of light is mediated by dopamine.
Exposure to high illuminances (15,000 lux) for 5 hours per day significantly slowed compensation for negative lenses, compared with that seen under 500 lux, although full compensation was still achieved.
High illuminance also reduced deprivation myopia by roughly 60%, compared with that seen under 500 lux. This protective effect was abolished, however, by the daily injection of spiperone, but was unaffected by the injection of a vehicle solution.
High illuminance also reduced deprivation myopia by roughly 60%, compared with that seen under 500 lux. This protective effect was abolished, however, by the daily injection of spiperone, but was unaffected by the injection of a vehicle solution.
High illuminance levels reduce the rate of compensation for negative lenses and enhance the rate for positive lenses, but do not change the set point of emmetropization (target refraction). The retardation of myopia development by light is partially mediated by dopamine, as the injection of a dopamine antagonist abolishes the protective effect of light, at least in the case of deprivation myopia."
From the full text:
"A possible interaction that should be considered is the change of pupil size in bright light. Schaeffel et al.27 found that the pupil size in chicks is reduced by roughly 50% of its maximum diameter under an illuminance of only 1000 lux. It is clear that a smaller pupil size increases the depth of focus and may therefore diminish the error signal driving emmetropization. However, changes in depth of focus cannot explain why bright light accelerated compensation for positive lenses. Furthermore, the development of deprivation myopia was also significantly suppressed under bright light, even though depth of focus does not play a role under the diffusers. In summary, changes in depth of focus cannot explain the effects of high illuminance on compensation for imposed defocus. Pupil constriction apparently also has no effect on refractive development in the uncovered fellow eyes.
Exposure to high illuminance levels reduces the rate of ocular growth normally seen in response to the fitting of negative lenses or translucent diffusers, and enhances the growth suppression of plus lenses, but does not alter normal ocular development. Further, the protective effect of light against the development of myopia appears to be mediated by dopamine, as the injection of a dopamine D2-specific antagonist abolishes the protective effect of light, at least in the case of deprivation myopia."
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From the full text:
"A possible interaction that should be considered is the change of pupil size in bright light. Schaeffel et al.27 found that the pupil size in chicks is reduced by roughly 50% of its maximum diameter under an illuminance of only 1000 lux. It is clear that a smaller pupil size increases the depth of focus and may therefore diminish the error signal driving emmetropization. However, changes in depth of focus cannot explain why bright light accelerated compensation for positive lenses. Furthermore, the development of deprivation myopia was also significantly suppressed under bright light, even though depth of focus does not play a role under the diffusers. In summary, changes in depth of focus cannot explain the effects of high illuminance on compensation for imposed defocus. Pupil constriction apparently also has no effect on refractive development in the uncovered fellow eyes.
Exposure to high illuminance levels reduces the rate of ocular growth normally seen in response to the fitting of negative lenses or translucent diffusers, and enhances the growth suppression of plus lenses, but does not alter normal ocular development. Further, the protective effect of light against the development of myopia appears to be mediated by dopamine, as the injection of a dopamine D2-specific antagonist abolishes the protective effect of light, at least in the case of deprivation myopia."
Link to the text
