Changes in Amacrine Cell Numbers and Morphology in Response To Induced Myopia and Hyperopia

S. T. Wong, J. Sivak, A. Bal, M. Callender, A.J. Bakelaar
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Abstract

Myopia and hyperopia have been artificially induced in animal models by various manipulations of their early visual environment. Ametropias have been produced using lid suture1, changing illumination levels (dark-rearing2, constant light3, dim lighting4), intra-ocular injections5, treatment with defocussing lenses6, and the application of translucent occluders7. Abnormal ocular growth appears to be a major factor that causes ametropia. Myopic eyes are enlarged, while hyperopic eyes are smaller compared to control eyes. Changes in the sclera8, choroid9, and orbital bone10 surrounding the affected eyes also reflect abnormal growth mechanisms. Various studies11,12,13 suggest that the signal or signals which control eye growth may arise from within the retina itself. It has been suggested that retinal amacrine cells play a role in mediating ocular growth8. This study examines how dopaminergic and serotonergic amacrine cells are quantitatively and qualitatively affected by induced myopia and hyperopia.
诱发性近视眼和远视后无毛细胞数量和形态的变化
在动物模型中,通过对其早期视觉环境的各种操纵,人工诱导出近视和远视。屈光不正的治疗方法包括眼睑缝合术、改变光照水平(暗养、恒定光照、昏暗光照)、眼内注射、离焦镜片治疗以及使用半透明封堵器。异常的眼部生长似乎是导致屈光不正的一个主要因素。近视眼放大,远视眼比对照眼小。受累眼睛周围的巩膜、脉络膜和眶骨的变化也反映了异常的生长机制。各种研究11,12,13表明,控制眼睛生长的信号可能来自视网膜本身。有人认为视网膜无突细胞在调节眼部生长中起作用8。本研究探讨了多巴胺能和血清素能无分泌细胞如何在数量和质量上受到诱发性近视眼和远视的影响。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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