Effects of wavelength on achieving and maintaining emmetropia

在眼睛还在生长的出生后发育过程中，一种“正视化机制”使用 眼屈光不正调节巩膜壳生长以使眼轴长度与焦点相匹配 飞机。尽管如此，在超过40%的美国人和高达96%的东亚群体中，眼睛变得太长了 因为它本身就是光学的，因此是短视的。即使是少量近视也会增加患失明的风险 条件和屈光手术不会改变这一点。因此，有效的策略来减缓眼睛的生长和 降低近视的患病率是必要的。 正视的维持是一个被忽视的研究领域。大多数近视儿童的正视率相对较高 正常情况下，但无法在较长的正视维持阶段维持正视。我们的 对树鼠(与灵长类动物关系密切的锥体主导的二色哺乳动物)的研究表明， 保持正视是整个青春期的一个活跃过程。眼睛是不是变得太短了 (远视)，并应增加其增长率以维持正视(需要视网膜GO信号)，或者是 变得太长(近视)，应该放慢眼轴延长率以维持正视(视网膜停止 需要信号)。一个重要的问题是，我们没有对视觉线索有一个坚实的理解 由正视化机制用来产生停止信号，以防止眼睛变得太 长。在树鼠身上，我们发现暴露在窄带长波(红色)光下(这只是 刺激长波敏感的视锥细胞)似乎会产生减缓生长的停止信号 在正视化的维护阶段。 在具体目标1中，我们将确定红灯产生最大值的最佳参数 在最小曝光的情况下停止信号并了解红灯停止信号是否显示非线性求和，类似于 产生停止信号的其他刺激(近视散焦或戴镜中断)。 在特定的目标2中，我们将确定红灯“处理”是否能产生一致的停止信号 在很长一段时间内处于正规化的维护阶段。我们还将检查红灯是否可以 在类似于近视控制研究中使用的范式中抵消负透镜的近视诱发效应。 在特定的目标3中，我们将使用视网膜多巴胺的分析，以及视网膜和 视网膜后信号级联，以确定红灯停止信号是否通过与其他信号相同的路径起作用 停止刺激(如从诱导近视中恢复)，或者如果路径是平行的和新颖的。 从这个项目中获得的知识不仅将产生关于 维护阶段的正视化机制，也可能导致RED的发展 光作为一种新的抗近视疗法。

During postnatal development when the eye is still growing, an “emmetropization mechanism” uses the eye’s refractive error to regulate the growth of the scleral shell to match the axial length of the eye to the focal plane. Despite this, in over 40% of Americans and up to 96% of groups in East Asia, the eye becomes too long for its own optics and is thus myopic. Even low amounts of myopia raise the risk of developing blinding conditions and refractive surgery does not change this. Thus, effective strategies to slow eye growth and reduce the prevalence of myopia are needed. Maintenance of emmetropia is a neglected area of research. Most myopic children emmetropize relatively normally, but then are unable to maintain emmetropia in the longer maintenance phase of emmetropia. Our research in tree shrews (cone-dominated dichromatic mammals closely related to primates) has shown that maintaining emmetropia is an active process throughout adolescence. Is the eye becoming too short (hyperopia) and should increase its growth rate to maintain emmetropia (retinal GO signals are needed), or is it becoming too long (myopia) and should slow the axial elongation rate to maintain emmetropia (retinal STOP signals are needed). An important problem is that we do not have a solid understanding of the visual cues used by the emmetropization mechanism to generate STOP signals that will prevent eyes from becoming too long. In tree shrews, we have discovered that exposure to narrow-band long wavelength (red) light (which only stimulates the long-wavelength sensitive, or LWS, cones) seems to generate STOP signals that slow growth during the maintenance phase of emmetropization. In specific aim 1, we will determine the optimal parameters for the red light to generate the maximum STOP signal with minimal exposure and learn if red-light STOP signals show non-linear summation, similar to other stimuli that generate STOP signals (myopic defocus or interrupted minus-lens wear). In specific aim 2, we will determine if the red light “treatment” can produce consistent STOP signaling over a long period of time in the maintenance phase of emmetropization. We will also examine if the red light can counteract the myopiagenic effects of a minus lens in a paradigm similar to that used in myopia-control studies. In specific aim 3, we will use both analysis of retinal dopamine, and of gene expression in the retina and post-retinal signaling cascade, to determine if red-light STOP signals act via the same pathways as other STOP stimuli (such as recovery from induced myopia), or if the pathways are parallel and novel. The knowledge gained from this project will not only generate critical data on the operation of the emmetropization mechanism during the maintenance phase, but also may result in the development of red light as a novel anti-myopia therapy.