The chick eye is able to change its refractive state by as much as 7 D by pushing the retina forward or pulling it back; this is effected by changes in the thickness of the choroid, the vascular tissue behind the retina and pigment epithelium. Chick eyes first made myopic by wearing diffusers and then permitted unrestricted vision developed choroids several times thicker than normal within days, thereby speeding recovery from deprivation myopia. Choroidal expansion does not occur when visual cues are reduced by dim illumination during the period of unrestricted vision. Furthermore, in chick eyes presented with myopic or hyperopic defocus by means of spectacle lenses, the choroid expands or thins, respectively, in compensation for the specific defocus imposed. Consequently, when the lenses are removed, the eye finds its refractive error suddenly of opposite sign, and the choroidal thickness again compensates by changing in the opposite direction. If a local region of the eye is made myopic by a partial diffuser and then given unrestricted vision, the choroid expands only in the myopic region. Although the mechanism of choroidal expansion is unknown, it might involve either a increased routing of aqueous humor into the uveoscleral outflow or osmotically generated water movement into the choroid. The latter is compatible with the increased choroidal proteoglycan synthesis either when eyes wear positive lenses or after diffuser removal.
In chicks, visual deprivation leads to myopia and enlargement of the vitreous chamber of the eye. When chicks were raised with white translucent occluders over their eyes so that either the nasal half, the temporal half, or all of the retina was visually deprived, the resulting myopia (median = -15 diopters) was limited to the deprived part of the retina, regardless of which half of the retina was visually deprived; the nondeprived part remained nearly emmetropic. Correspondingly, the vitreous chamber was elongated only in the region of the visual deprivation, resulting in eyes with different asymmetric shapes depending on which retinal region was deprived. These results argue for a local regulation of ocular growth that is dependent on vision and suggest a hypothesis to explain the epidemiological association of myopia in humans with large amounts of reading. Because most nonfoveal retinal neurons have large receptive fields, they cannot resolve the individual letters on the printed page; this may lead to their activity being less during reading than during most other forms of visual stimulation. Thus, the impoverished stimulus situation of reading may lead to myopia, as do other types of visual form deprivation.
Deprivation of form vision restricted to a region of the retina produces myopia and axial elongation only in that region. We asked whether this control of eye growth by the presence or absence of visual stimuli might take place entirely within the eye. Chicks with neonatal optic nerve section, wearing an occluder that deprived one half of the retina of form vision, had vitreous chamber elongation and myopia both restricted to the deprived region. Chicks with optic nerve section but without occluders had eyes smaller than normal with severe hyperopia. These results suggest that two different mechanisms may control eye growth, one within the eye and the other in the brain.
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