Ma Ziyan, Jeong Heonuk, Yang Yajing, Jiang Xiaoyan, Ikeda Shin-Ichi, Negishi Kazuno, Kurihara Toshihide, Tsubota Kazuo
Laboratory of Photobiology, Keio University School of Medicine, Tokyo, Japan.
Department of Ophthalmology, Keio University School of Medicine, Tokyo, Japan.
Ophthalmic Physiol Opt. 2023 May;43(3):558-565. doi: 10.1111/opo.13125. Epub 2023 Mar 17.
Apart from genetic factors, recent animal studies on myopia have focused on localised mechanisms. In this study, we aimed to examine the contralateral effects of monocular experimental myopia and recovery, which cannot be explained by a mere local mechanism.
One eye of 3-week-old C57BL/6 male mice was fitted with a -30 dioptre (D) lens. The mice were distributed into two groups based on different conditions in the contralateral eye: either no lens (NLC) (n = 10) or a Plano lens on the contralateral eye (PLC) group (n = 6). Mice receiving no treatment on either eye were set as a control group (n = 6). Lenses were removed after 3 weeks of myopia induction. All mice were allowed to recover for 1 week in the same environment. Refractive status, axial length (AL) and choroidal thickness were measured before myopia induction, after 1 and 3 weeks of lens wear and after 1 week of recovery.
One week after removing the lenses, complete recovery was observed in the eyes that wore the -30 D lenses. In both the PLC and NLC groups, the refractive status showed a myopic shift after lens removal. Additionally, the choroid was significantly thinned in these eyes. The -30 D wearing eye showed a significant increase in AL after 3 weeks of lens wear. While the AL of the -30 D wearing eye ceased to grow after the lens was removed, the AL in the PLC and NLC contralateral eyes increased, and the binocular ALs gradually converged.
Recovery of lens-induced myopia was observed in mouse models. In the fellow eyes, the effects, including thinning of the choroid and changes in refractive status, were triggered by contralateral visual cues.
除遗传因素外，近期关于近视的动物研究主要集中在局部机制上。在本研究中，我们旨在研究单眼实验性近视及其恢复的对侧效应，这无法单纯用局部机制来解释。
给3周龄C57BL/6雄性小鼠的一只眼睛佩戴-30屈光度（D）的透镜。根据对侧眼的不同情况将小鼠分为两组：对侧眼不戴透镜（NLC）组（n = 10）和对侧眼戴平光透镜（PLC）组（n = 6）。两只眼睛均未接受治疗的小鼠作为对照组（n = 6）。在诱导近视3周后摘除透镜。所有小鼠在相同环境中恢复1周。在近视诱导前、佩戴透镜1周和3周后以及恢复1周后测量屈光状态、眼轴长度（AL）和脉络膜厚度。
摘除透镜1周后，佩戴-30 D透镜的眼睛观察到完全恢复。在PLC组和NLC组中，摘除透镜后屈光状态均出现近视性偏移。此外，这些眼睛的脉络膜明显变薄。佩戴-30 D透镜的眼睛在佩戴透镜3周后AL显著增加。虽然摘除透镜后佩戴-30 D透镜的眼睛的AL停止增长，但PLC组和NLC组对侧眼的AL增加，双眼AL逐渐趋于一致。
在小鼠模型中观察到透镜诱导性近视的恢复。在对侧眼中，包括脉络膜变薄和屈光状态改变在内的效应是由对侧视觉线索触发的。
