Institute of Neurobiology, Institutes of Brain Science, State Key Laboratory of Medical Neurobiology and Collaborative Innovation Center for Brain Science, Fudan University, Shanghai, China.
Jiangsu Key Laboratory of Neurodegeneration, Department of Pharmacology, Nanjing Medical University, Nanjing, Jiangsu, China.
Invest Ophthalmol Vis Sci. 2015 Jan 20;56(2):967-77. doi: 10.1167/iovs.13-13362.
Retinal dopamine has been long implicated in the signaling pathway regulating eye growth, as evidenced by its reduced levels in myopic eyes in various species. We examined whether and how retinal dopamine levels were changed in a C57BL/6 mouse model of experimental myopia.
Form-deprivation myopia (FDM) was induced in C57BL/6 mice by wearing monocular occluder for 4 weeks. Refractive errors were measured using an infrared photorefractor. Retinal dopamine/DOPAC and vitreal DOPAC levels were assessed by high-performance liquid chromatography (HPLC). Extracellular dopamine concentrations were examined by Western blot analysis of dopamine transporter (DAT) expression levels. The intactness of retinal dopaminergic system was evaluated by counting tyrosine hydroxylase (TH) immunoreactive cells, measuring the areas occupied by processes of these cells, and quantifying retinal TH expression at both protein and transcription levels.
Form-deprivation myopia was successfully induced in C57BL/6 mice with the refractive status of deprived eyes being significantly different from fellow eyes. Unlike most of the previous results obtained in other myopic animal models, however, no significant changes in retinal dopamine, DOPAC, DAT, and vitreal DOPAC levels were detected in deprived eyes, either in the daytime or at night. Furthermore, neither the number of dopaminergic amacrine cells, the area size occupied by the processes of these cells, nor retinal TH expression, were altered in deprived eyes.
The retinal dopamine system remains intact in C57BL/6 mice with FDM, and retinal dopamine levels are not associated with the development of FDM in this mouse strain.
视网膜多巴胺在调节眼球生长的信号通路中一直被认为起着重要作用，这一点在多种物种的近视眼中其水平降低得到了证明。我们研究了实验性近视的 C57BL/6 小鼠模型中视网膜多巴胺水平是否发生了变化以及如何发生变化。
通过佩戴单眼眼罩 4 周诱导 C57BL/6 小鼠形成形觉剥夺性近视（FDM）。使用红外视网膜折射仪测量屈光度。通过高效液相色谱法（HPLC）评估视网膜多巴胺/DOPAC 和玻璃体内 DOPAC 水平。通过 Western blot 分析多巴胺转运蛋白（DAT）表达水平来检查细胞外多巴胺浓度。通过计数酪氨酸羟化酶（TH）免疫反应性细胞、测量这些细胞过程占据的面积以及定量视网膜 TH 蛋白和转录水平表达来评估视网膜多巴胺能系统的完整性。
成功在 C57BL/6 小鼠中诱导了形觉剥夺性近视，与未受影响的眼睛相比，受影响眼睛的屈光状态明显不同。然而，与在其他近视动物模型中获得的大多数先前结果不同的是，无论是在白天还是在夜间，受影响眼睛中的视网膜多巴胺、DOPAC、DAT 和玻璃体内 DOPAC 水平均未发生显著变化。此外，受影响眼睛中的多巴胺能无长突细胞数量、这些细胞过程占据的面积大小或视网膜 TH 表达均未改变。
在 FDM 的 C57BL/6 小鼠中，视网膜多巴胺系统保持完整，并且在该小鼠品系中，视网膜多巴胺水平与 FDM 的发展无关。
