MYOPIA & OCULAR GROWTH--NEURAL MECHANISMS

拟议的研究试图澄清神经和/或生化 控制出生后眼部生长和青光眼发育的机制 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Clear 对眼睛生长的神经药理作用使这成为一个合理的目标。在……里面 雏猴，幼猴，很可能在人类中，依赖于视觉的反馈 影响出生后眼部生长的机制，从而牵涉到神经 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 视网膜和近视雏鸡视网膜中受抑制的多巴胺构成 首次发现实验性近视的神经化学改变。 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伸长 近视的特点还可以改变其形状。扩展这些功能 研究发现，胆碱能药物也会影响肿瘤的生长 轴向维度上的小鸡眼。 我们希望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 对眼睛生长和屈光的调节机制的理解 状态。以雏鸟为模型，研究将定向到 以下方面：1)进一步界定多巴胺在眼部的作用 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，并应继续研究局部的影响 应用的多巴胺制剂。2)澄清胆碱能对眼睛的影响 成长。除了扩大我们的药理发现，我们还将启动 生化和组织化学研究。3)识别其他 控制眼睛生长和屈光不正的机制。在寻找其他 可能的神经机制，我们将重点介绍周围神经 系统和神经肽。 通过协调药理、生化、组织化学和解剖学 方法，我们试图阐明控制眼睛生长的机制， 正视化与近视的发展。我们希望这些研究 最终将导致对人类近视的更好的理解，并 可行的药物治疗以防止其发展。

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.