Abstract
Studies on developing mammalian as well as avian eyes have suggested the existence of an emmetropization process that matches axial length to focal length. A vision-dependent signal may slow axial elongation to hold the retina in the focal plane: deprivation of clear images on the retina produces an elongated, myopic eye in humans, most monkeys, and in tree shrews. If deprivation is removed in young, experimentally myopic tree shrews, recovery can occur due partially to slowing of axial expansion relative to the continued increase in focal length of the developing eye. In at least some mammals, it seems that a retinal signal is transmitted directly to the choroid and/or sclera; deprivation-induced myopia can develop despite blocking ganglion cell output to central brain structures. In tree shrews, as in avians, this signal seems local: deprivation in part of the visual field produces elongation and myopia selectively in the deprived region of the eye. Although accommodation may participate in normal ocular development, experimental myopia can develop in tree shrews despite atropine sulfate administration. In mammals it is still unclear whether the emmetropization process controls ocular growth, stretch, or both. How emmetropization is disrupted in human myopia also remains uncertain.
© 1991 Optical Society of America
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