The many studies reporting myopia in response to form deprivation (either with diffusers or lid suture) provide convincing evidence for an effect of visual experience on ocular development. More significantly, there is compelling evidence based on studies involving spectacle lenses that vision actively directs eye growth; specifically, negative lenses which impose hyperopic defocus cause eyes to grow toward myopia, whereas eyes with myopic defocus imposed by positive lenses grow toward hyperopia. These growth changes include choroidal and scleral components, both of which serve to reduce the imposed defocus, a process known as emmetropization. In addition, there appears to be another process that keeps the two eyes yoked (coupled) together such that compensatory growth changes in one eye cause the other eye to change its growth in the same direction, although to a lesser extent. We understand very little about these two mechanisms, yet both are potentially of great clinical significance. Understanding emmetropization may provide the key to preventing myopia in humans. Understanding interocular yoking may help us to understand anisometropia (i.e. the two eyes have different refractions), a common condition in infants. In relation to emetropization, this proposal asks whether the brain is involved. The brain seems not to be required in the case of form deprivation myopia as optic nerve section does not prevent it. However, this is unclear in the case of the lens-induced changes. By interfering with eye-brain communication, I propose to resolve this important issue for the choroidal and scleral components of emmetropization. If preliminary results are confirmed indicating that the brain does play a role, I will try to identify the pathways involved using selective lesioning of the most likely efferent pathways. In relation to interocular yoking in eye growth, this proposal seeks to clarify the conditions under which these interactions occur. I will also assess how the refractive state of each of the eyes (natural or altered experimentally), influences their interactions. If the existence of yoking is confirmed, I propose to identify the pathways involved, again using a selective lesioning approach.
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