MECHANISMS OF OCULAR DEVELOPMENT

眼睛发育的机制

• 批准号: 3261625
• 负责人: THOMAS T NORTON
• 金额: $ 12.86万
• 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 1994-03-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/3261625
• 关键词: beta antiadrenergic agent; ciliary ganglion; extraocular muscle; eye; eye accommodation; eye disorder diagnosis; eye refraction disorder; eyelids; growth /development; intraocular pressure; myopia; neural information processing; sclera; visual deprivation; visual feedback

It has been found that some animal species become myopic when an eye is exposed to visual deprivation during postnatal development. This environmentally-produced alteration in ocular development can provide information about the mechanisms that normally act to produce emmetropic and ametropic eyes. Studies ar proposed in the present application on a mammalian animal model, thee shrew, to answer several questions: 1) Are there active regulatory mechanism that produce emmetropia? 2) What is the role of accommodation in any regulatory mechanism? 3) Are there local retinal control mechanisms within the eye that do not require a feedback loop through central visual structures? 4) When an eye becomes myopic as a result of environmental manipulations, is the axial elongation due to growth or stretch? Experiment 1 will determine whether rearing with + or - power goggles will result in shorter or longer eyes. In addition, we will explore whether recovery from experimentally-induced myopia can occur after small amounts of myopia have been produced early in the sensitive period. Experiment 2 will determine whether experimentally-induced myopia can develop after removal of accommodation by lesions of either the Edinger-Westphal nucleus or the ciliary ganglion. Experiment 3 will determine whether local retinal control mechanisms exist that can regulate the development of the eye. In these experiments, we will test whether local myopia can result from partial visual field deprivation, whether exposure to strobe-light flashes will prevent lid-suture myopia, and whether lid-suture myopia develops during blockage of afferent visual information with intravitreal tetrodotoxin. Experiment 4 will examine whether the axial elongation in lid-suture myopia occurs through stretch of the sclera as suggested by preliminary data using lathyritic agents to enhance the experimentally-induced myopia. It will also provide a needed dark-rearing control for the lathyritic studies. If the experiments support scleral stretch as a mechanism, in Experiment 5 we will reduce intraocular pressure to determine whether this will decrease the amount of lid-suture myopia. These experiments will significantly advance our understanding of the mechanisms that affect ocular development. If we can learn the mechanisms that produce emmetropia and ametropia in tree shrews, a species closely related to primates, it will then be reasonable to ask whether similar mechanisms control ocular development in humans.

已经发现，当某些动物物种成为近视 眼睛在产后发育过程中暴露于视觉剥夺。 这种环境产生的眼部发展改变可以 提供有关通常行动到的机制的信息 产生膜状和非洲眼睛的眼睛。 研究中提出的 当前在哺乳动物动物模型上应用Thee Shrew， 回答几个问题：1）是否有主动调节机制 产生艾美特罗尼亚？ 2）住宿的作用是什么 有监管机制吗？ 3）是否存在局部视网膜控制 眼中的机制不需要反馈循环 通过中央视觉结构？ 4）当眼睛变成近视时 由于环境操纵的结果是轴向伸长 由于生长还是伸展？ 实验1将确定是否使用 +或 - 功率饲养 护目镜将导致更短或更长的眼睛。 另外，我们 将探索是否从实验引起的近视中恢复 早期产生少量近视后可能发生 在敏感时期。 实验2将确定是否 实验引起的近视可以在去除后发展 通过埃丁 - 韦斯特法核的病变或 睫状神经节。 实验3将确定是否本地 存在视网膜控制机制可以调节发展 眼睛。 在这些实验中，我们将测试是否本地 近视可能是由于部分视野剥夺而导致的 暴露于频闪的闪光灯会防止盖透明胶近视， 以及盖 - 缝合近视是否在阻塞过程中发展 玻璃体内四毒素的视觉信息。 实验4 将检查盖孔近视中的轴向伸长率是否 如初步所建议的 使用lathyritic剂的数据来增强实验诱导的 近视。 它还将为 latheritic研究。 如果实验支持巩膜拉伸 一种机制，在实验5中，我们将降低人眼压 为了确定这是否会减少盖子的量 近视。 这些实验将大大提高我们对 影响眼部发育的机制。 如果我们可以学习 在树sh中产生艾米特罗比亚和阿图罗皮的机制， 与灵长类动物密切相关的物种，这将是合理的 询问类似机制是否控制着眼部发展 人类。