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According to the Centers for Disease Control, the most frequent ocular condition afflicting the United States population is refractive error. In most instances, refractive error occurs due to an improper match between the axial length of the eye and objects at optical infinity (i.e., myopia, hyperopia or astigmatism) or due to the loss of ability to focus on near objects with age (presbyopia). The ability of the eye to coordinate growth of the organ while the organism physically matures is of particular interest to vision scientists. In humans, this relationship appears to be changing as the prevalence of refractive errors, particularly myopia, increases. This alteration in the regulation on ocular growth can be detrimental, as myopia is associated with potentially blinding diseases such as glaucoma, retinal detachment, retinoschesis and myopic retinal degeneration. A number of potential mechanisms have been proposed for why the prevalence of myopia is on the rise; however, our knowledge of ocular growth regulation is incomplete. Further insight into how ocular growth is regulated may help scientists and clinicians develop effective therapeutic interventions to slow, or possibly prevent, myopia development.Chapter 1 of the dissertation addresses the significant literature regarding the development of myopia in experimental animals, with an emphasis on the role of unobstructed vision in normal refractive development and potential mechanisms involved in regulating ocular growth. Chapter 2 of the dissertation examines the role of Insulin-like Growth Factor 1 (IGF1) and Fibroblast Growth Factor 2 (FGF2) in the regulation of ocular growth. Recent research implicates insulin as a potent stimulator of ocular growth. In chickens, a combination of IGF1 & FGF2 radically alters ocular growth, leading to increased intraocular pressure, axial length and anterior chamber changes leading to the development of extreme myopia. Chapter 3 examines the expression of guanine-nucleotide binding protein β3 (GNB3), also known as cone β-transducin, in multiple species. We demonstrate that a mutant chicken model with congenital reduction in vision, the Retinopathy, Globe Enlarged (RGE), lacks GNB3 in retinal neurons critical for normal visual signal transduction. Chapter 4 of the dissertation examines whether the RGE chicken can respond to experimental visual manipulations known to cause ocular growth and myopia in multiple animal species. The dissertation concludes with Chapter 5, a discussion of the pertinence of the finding of this research and proposed future avenues of investigation to further our understanding of regulation of ocular growth. |
