Karouta Cindy, Thomson Kate, Morgan Ian, Ashby Regan
Biomedical Science, Faculty of Science and Technology, University of Canberra, ACT, Australia.
Research School of Biology, Australian National University, ACT, Australia.
Ophthalmol Sci. 2025 Mar 28;5(5):100779. doi: 10.1016/j.xops.2025.100779. eCollection 2025 Sep-Oct.
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.
An experimental study.
White Leghorn chickens ().
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.
Refraction (infrared photoretinoscopy), axial length (A-scan ultrasonography), and DA levels (liquid chromatography-tandem mass spectrometry).
Bright light inhibited LIM in an intensity-dependent manner ( < 0.05) but did not prevent full compensation. The protection afforded by bright light was significantly reduced by administration of spiperone (D2-like, < 0.05), but not SCH-23390 (D1-like, = 0.77). Retinal DA levels showed an intensity-dependent increase ( < 0.05).
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.
Proprietary or commercial disclosure may be found in the Footnotes and Disclosures at the end of this article.
有假设认为,户外活动时间能够预防人类近视的发生,其根本原因在于受到强光照射。与此观点相符的是,在所有已研究的物种中,强光均能抑制形觉剥夺性近视(FDM)的发展。虽然在大多数物种中,强光也能抑制晶状体诱导性近视(LIM),但目前尚不清楚这种抑制作用是否存在强度依赖性,以及多巴胺(DA)在该模型中是否与在FDM中一样发挥关键作用。
一项实验研究。
白来航鸡()。
为研究光照对LIM的影响,给佩戴-10屈光度镜片的雏鸡分别照射500、20000或40000勒克斯的光线,持续14天(每组n = 6)。为评估DA的作用,在6种光照强度(从黑暗到40000勒克斯)下,对先前暗适应的动物在光照30分钟后测量其DA水平。在另一项实验中,对佩戴负镜片且处于40000勒克斯光照下的雏鸡(每组n = 5至6)每日一次给予D1样(SCH-23390)或D2样(螺哌隆)受体拮抗剂,持续5天。
屈光(红外视网膜检影法)、眼轴长度(A超超声检查)和DA水平(液相色谱 - 串联质谱法)。
强光以强度依赖性方式抑制LIM(<0.05),但不能完全阻止代偿。给予螺哌隆(D2样,<0.05)可显著降低强光提供的保护作用,但给予SCH-23390(D1样,= 0.77)则无此作用。视网膜DA水平呈现强度依赖性升高(<0.05)。
如先前在FDM中观察到的那样,强光可强度依赖性地抑制LIM的发展。这种保护作用至少部分是通过DA依赖性机制实现的。然而,强光无法阻止对负镜片的代偿,这表明两种近视实验模型之间存在机制差异。这些差异很可能与LIM中存在而FDM中不存在的散焦驱动的生长终点有关。
在本文末尾的脚注和披露中可能会找到专有或商业披露信息。