MYOPIA & OCULAR GROWTH--NEURAL MECHANISMS

拟议的研究旨在澄清神经和/或生物化学 控制出生后眼部生长和发育的机制 近视（近视）良好的实验模型，视网膜的证据 参与监管过程和发现明确的 对眼睛生长的神经药理学作用使其成为合理的目标。 在 小鸡、幼猴和人类都可能存在视觉依赖性反馈 机制影响出生后的眼睛生长，因此涉及神经 控制眼睛大小和屈光不正的机制。 我们最近 近视猴血管活性肠肽升高的观察 视网膜和近视小鸡视网膜中的多巴胺抑制构成了 实验性近视中神经化学改变的首次鉴定。 我们的后续药理学研究表明，局部应用 多巴胺能药物不仅可以防止轴向延长， 近视的特点，而且还可以修改其形状。 扩大这些 研究中，我们发现胆碱能药物也会影响 鸡眼的轴向尺寸。 我们寻求更详细地了解这些神经化学物质和 神经药理学观察可以整合到一个改进的 了解调节眼睛生长和屈光的机制 status. 使用小鸡作为模型，研究将被引导到 以下方面：1）进一步明确多巴胺在眼内的作用， 生长控制和屈光不正的发展。 我们将寻求 视网膜多巴胺与实验条件的进一步相关性 影响眼睛生长，并将继续研究局部 应用多巴胺药物。 2)阐明胆碱能对眼睛的影响 增长 除了扩大我们的药理学发现，我们将启动 生化和组织化学研究。 3)查明其他 调节眼睛生长和屈光不正的机制。 在寻求其他 可能的神经机制，我们将强调周围神经 系统和神经肽。 通过协调药理学、生物化学、组织化学和解剖学 方法，我们试图阐明控制眼生长的机制， 正视化和近视的发展。 我们希望这些研究 最终将导致对人类近视的更好理解， 可行的药物治疗来防止其发展。

The proposed research seeks clarification of neural and/or biochemical mechanisms that control postnatal ocular growth and the development of myopia (nearsightedness) good experimental model, evidence of retinal participation in the regulatory process and discovery of clear neuropharmacological effects on eye growth make this a reasonable goal. In the chick, juvenile monkey and likely in man, a vision-dependent feedback mechanisms influences postnatal ocular growth, hence implicating neural mechanisms in control of eye size and refractive error. Our recent observations of elevated vasoactive intestinal peptide in the myopic monkey retina and depressed dopamine in the myopic chick retina constitute the first identifications of neurochemical alterations in experimental myopia. Our follow-up pharmacological studies demonstrate that local application of dopaminergic agents not only can prevent the axial elongation characteristic of myopia but also can modify its shape. Expanding these studies, we have found that cholinergic agents also influence the growth of the chick eye in the axial dimension. We seek a more detailed understanding of how these neurochemical and neuropharmacological observations can be integrated into an improved understanding of the mechanisms that regulate ocular growth and refractive status. Using the chick as a model, studies will be directed to the following areas: 1) Further definition of the role of dopamine in ocular growth control and the development of refractive errors. We shall seek further correlates of retinal dopamine with experimental conditions influencing eye growth and shall continue to study the influence of locally applied dopamine agents. 2) Clarification of cholinergic influences on eye growth. Besides expanding our pharmacological findings, we shall initiate biochemical and histochemical studies. 3) Identification of other mechanisms governing ocular growth and refractive error. In seeking other possible neural mechanisms, we shall emphasize the peripheral nervous system and neuropeptides. By coordinating pharmacological, biochemical, histochemical and anatomical methods, we seek to clarify mechanisms controlling ocular growth, emmetropization and the development of myopia. We hope that these studies ultimately will lead to an improved understanding of human myopia and to a viable drug therapy to prevent its development.