Light Inhibits Lens-Induced Myopia through an Intensity-Dependent Dopaminergic Mechanism

IF 3.2 Q1 OPHTHALMOLOGY

Ophthalmology science Pub Date : 2025-03-28 DOI:10.1016/j.xops.2025.100779

Cindy Karouta PhD , Kate Thomson PhD , Ian Morgan PhD , Regan Ashby PhD

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Abstract

Purpose

Bright light exposure has been postulated to underlie the ability of time spent outdoors to prevent the development of myopia in humans. In support of this, bright light inhibits the development of form-deprivation myopia (FDM) in all species studied. While lens-induced myopia (LIM) is also inhibited by bright light in most species, it remains unclear whether this is brought about in an intensity-dependent manner and whether dopamine (DA) plays the same critical role in this paradigm as is seen in FDM.

Design

An experimental study.

Subjects

White Leghorn chickens (Gallus gallus).

Methods

To examine the effect of light on LIM, chicks fit with lenses of −10 diopters were exposed to 500, 20 000, or 40 000 lux for 14 days (n = 6 per group). To assess the role of DA, its levels were measured 30 minutes after light exposure in previously dark-adapted animals over 6 light intensities (between dark and 40 000 lux). In a separate experiment, a D1-like (SCH-23390) or D2-like (spiperone) receptor antagonist was administered (once daily) to chicks wearing negative lenses under 40 000 lux (n = 5 to 6 per group) for a period of 5 days.

Main Outcome Measures

Refraction (infrared photoretinoscopy), axial length (A-scan ultrasonography), and DA levels (liquid chromatography-tandem mass spectrometry).

Results

Bright light inhibited LIM in an intensity-dependent manner (P < 0.05) but did not prevent full compensation. The protection afforded by bright light was significantly reduced by administration of spiperone (D2-like, P < 0.05), but not SCH-23390 (D1-like, P = 0.77). Retinal DA levels showed an intensity-dependent increase (P < 0.05).

Conclusions

As previously observed for FDM, bright light can inhibit the development of LIM in an intensity-dependent manner. This protection occurs, at least in part, via a DA-dependent mechanism. However, bright light's inability to prevent compensation to negative lenses is indicative of mechanistic differences between the 2 experimental models of myopia. These differences are most likely linked to the presence of a defocus-driven end point for growth in LIM that is not present in FDM.

Financial Disclosure(s)

Proprietary or commercial disclosure may be found in the Footnotes and Disclosures at the end of this article.

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光通过强度依赖的多巴胺能机制抑制晶状体诱发的近视

目的：人们认为，暴露在强光下可能是户外活动时间预防人类近视的基础。为了支持这一点，在所有被研究的物种中，明亮的光线抑制了形式剥夺性近视（FDM）的发展。虽然在大多数物种中，晶状体诱发性近视（LIM）也受到强光的抑制，但尚不清楚这是否以强度依赖的方式发生，以及多巴胺（DA）是否在这种范式中扮演与FDM相同的关键角色。设计：实验研究。实验对象：白来窝鸡。方法为了研究光照对LIM的影响，将配戴- 10屈光度透镜的雏鸡分别暴露于50、20、40 000勒克斯环境14天（每组6只）。为了评估DA的作用，在先前适应黑暗的动物中，在6个光强度（黑暗至40000勒克斯）的光照下暴露30分钟后测量其水平。在另一项试验中，给戴阴性镜片的雏鸡（每组5 ~ 6只，光照40000勒克斯）注射d1样（SCH-23390）或d2样（spiperone）受体拮抗剂（每天1次），持续5天。主要观察指标：折射（红外视网膜镜）、轴向长度（a -超声扫描）和DA水平（液相色谱-串联质谱）。结果强光对LIM的抑制呈强度依赖性(P <；0.05)，但不妨碍全额补偿。强光对小鼠的保护作用被施给spiperone (D2-like, P <；0.05)，而SCH-23390没有（d1样，P = 0.77）。视网膜DA水平呈强度依赖性升高(P <；0.05)。结论与先前观察到的FDM一样，强光可以以强度依赖的方式抑制LIM的发展。这种保护至少在一定程度上是通过依赖于da的机制实现的。然而，强光无法阻止负晶状体的补偿，这表明了两种实验近视模型之间的机制差异。这些差异很可能与LIM中存在散焦驱动的生长终点有关，而FDM中不存在这种终点。财务披露专有或商业披露可在本文末尾的脚注和披露中找到。

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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