MECHANISMS OF OCULAR DEVELOPMENT

眼睛发育的机制

• 批准号: 2391677
• 负责人: THOMAS T NORTON
• 金额: $ 24.69万
• 依托单位: UNIVERSITY OF ALABAMA AT BIRMINGHAM
• 依托单位国家: 美国
• 财政年份: 1986
• 资助国家: 美国
• 起止时间: 1986-04-01 至 1999-03-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/2391677
• 关键词: Scandentia; eye; eye accommodation; eye circulation; eye refraction disorder; growth /development; myopia; neural information processing; sclera; visual deprivation

Recent studies in tree shrew, a mammal closely related to primates, and in other species suggest that a mechanism normally operates during ocular development to coordinate the axial length of the eye with the focal length provided by the cornea and lens, producing emmetropia. Disruption of this mechanism with deprivation of visual forms results in an elongated, myopic eye. The goal of this project is to understand the mechanism that normally guides developing eyes toward emmetropia. The proposed experiments will explore three questions that derive from our past work on emmetropization: 1) what type of retinal signal(s) may be produced by defocussed images on the retina, 2) how do the signal(s) for control of ocular elongation cross from the retina via the choroid to the sclera and 3) how is the sclera remodelled to control elongation of the eye? Specifically, we will: 1) test our hypothesis that the emmetropization mechanism in tree shrew is a"1-way" mechanism able only to detect defocus and not a "2-way" mechanism able to differentiate between "myopic defocus" (focal plane in front of the retina) and "hyperopic defocus" (focal plane behind the retina), 2) investigate whether there are changes in choroidal blood flow in deprived myopic eyes that might participate in the communication of signals from retina to sclera and 3) examine mechanical, morphological and biochemical changes in the sclera that occur during normal development, induced myopia and recovery from myopia. The proposed experiments will significantly advance our understanding of the emmetropization mechanism. This, in turn, can help us to learn how human emmetropization normally occurs and how disruptions in the emmetropization mechanism may lead to human myopia and hyperopia.

最近在Tree Shrew的研究，一种与灵长类动物密切相关的哺乳动物， 在其他物种中，一种通常在眼期间起作用的机制 开发以协调眼睛的轴向长度与局灶性 由角膜和镜头提供的长度，产生艾米特罗尼亚。 破坏 剥夺视觉形式的这种机制导致 伸长，近视眼。 该项目的目的是了解 通常指导眼睛向艾米特罗尼亚发展的机制。 这 拟议的实验将探讨从我们的三个问题 过去的弹性化工作：1）可能是哪种类型的视网膜信号 通过视网膜上的dyocusted图像制作，2） 控制眼伸长从视网膜通过脉络膜到 巩膜和3）如何重塑巩膜以控制伸长率 眼睛？具体来说，我们将：1）检验我们的假设 树sh中的弹性化机制仅是一种“ 1向”机制 检测散焦，而不是能够区分的“ 2向”机制 在“近视散焦”之间（视网膜前的焦平面）和 “触角散焦”（视网膜后面的焦平面），2）研究 被剥夺的近视眼中脉络膜血流是否有变化 这可能参与从视网膜到的信号通信 巩膜和3）检查机械，形态和生化变化 在正常发育过程中发生的巩膜中，诱导近视和 从近视恢复。 提出的实验将大大提高我们对 弹性化机制。 反过来，这可以帮助我们了解 人类的燃料化通常会发生以及如何破坏 弹性化机制可能导致人类近视和远视。