We have been studying an animal model of myopia that holds great promise for inquiries into the cellular mechanisms of the anatomical changes responsible for the myopia and into the physiological mechanisms that cause these changes. This experimental myopia, which is produced by restricting the vision of a chick eye to the frontal visual field, develops very rapidly--changes are detectable in two days--and is quite severe--25 diopters of myopia is typical after two weeks. It seems to require the accommodation system since ciliary nerve section protects the eye from the myopia. We propose, first, to study the role of axial length of the eye and of its refractive components in this myopia at different stages of progression by means of ultrasound measurements for the axial dimensions of the eye, and measurements of corneal and lenticular curvatures. We will attempt to understand these anatomical changes in terms of cell division (measured by DNA synthesis), protein synthesis or histological architecture. Next, we plan to clarify the role of accommodation in this experimental myopia both by preventing accommodation pharmacologicallyand with lesions of the Edinger-Westphal nucleus and by manipulating it with electrical stimulation of its neural substrates and by behavioral control. We plan to investigate the physiological mechanisms that could intervene between the etiological factors and their anatomical sequelae by studies of changes in vitreous composition and in intraocular pressure. Finally, we are interested in testing the hypothesis that there exists a postnatal developmental regulatory mechanism that uses visual information to direct growth of the eye toward emmetropia and that interference with this mechanism may result in myopia. The understanding of the processes that result in myopia which could be derived from experiments on a model system such as the one studied here could have considerable value in suggesting new therapeutic and preventive approaches to myopia.
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