State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Institutes of Brain Science, Department of Neurology and Department of Ophthalmology, Zhongshan Hospital, Fudan University, Shanghai, China.
State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Institutes of Brain Science, Department of Neurology and Department of Ophthalmology, Zhongshan Hospital, Fudan University, Shanghai, China; Discipline of Neuroscience and Department of Anatomy and Physiology, College of Basic Medical Sciences, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Brain Res. 2020 Jan 1;1726:146537. doi: 10.1016/j.brainres.2019.146537. Epub 2019 Oct 28.
Higher visual centers could modulate visually-guided ocular growth, in addition to local mechanisms intrinsic to the eye. There is evidence that such central modulations could be species (even subspecies)-dependent. While the mouse has recently become an important experimental animal in myopia studies, it remains unclear whether and how visual centers modulate refractive development in mice, an issue that was examined in the present study. We found that optic nerve crush (ONC), performed at P18, could modify normal refractive development in the C57BL/6 mouse raised in normal visual environment. Unexpectedly, sham surgery caused a steeper cornea, leading to a modest myopic refractive shift, but did not induce significant changes in ocular axis length. ONC caused corneal flattening and re-calibrated the refractive set-point in a bidirectional manner, causing significant myopic (<-3 D, 54.5%) or hyperopic (>+3 D, 18.2%) shifts in refractive error in most (totally 72.7%) animals, both due to changes in ocular axial length. ONC did not change the density of dopaminergic amacrine cells, but increased retinal levels of dopamine and DOPAC. We conclude that higher visual centers are likely to play a role in fine-tuning of ocular growth, thus modifying refractive development in the C57BL/6 mouse. The changes in refractive error induced by ONC are accounted for by alternations in multiple ocular dimensions, including corneal curvature and axial length.
高级视觉中枢除了对眼睛的固有局部机制外,还可以调节视觉引导的眼球生长。有证据表明,这种中枢调节可能依赖于物种(甚至亚种)。虽然老鼠最近已成为近视研究中的重要实验动物,但仍不清楚视觉中枢是否以及如何调节老鼠的屈光发育,本研究对此进行了探讨。我们发现,在 P18 时进行视神经挤压(ONC)可以改变正常视觉环境下 C57BL/6 小鼠的正常屈光发育。出乎意料的是,假手术导致角膜陡峭,导致适度的近视屈光改变,但不会引起眼轴长度的显著变化。ONC 导致角膜变平,并以双向方式重新校准屈光设定点,导致大多数(总共 72.7%)动物的屈光误差发生显著的近视(<-3D,54.5%)或远视(>+3D,18.2%)变化,这两种情况均归因于眼轴长度的变化。ONC 并未改变多巴胺能无长突细胞的密度,但增加了视网膜中的多巴胺和 DOPAC 水平。我们得出结论,高级视觉中枢可能在调节眼球生长方面发挥作用,从而改变 C57BL/6 小鼠的屈光发育。ONC 引起的屈光误差变化归因于多个眼部尺寸的改变,包括角膜曲率和眼轴长度。