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目的观察在持续高眼压状态下大鼠外侧膝状体(lateral geniculate nucleus,LGN)细胞结构的变化及其与视神经纤维丢失的关系。方法通过烧灼大鼠巩膜表层静脉诱导建立大鼠慢性高眼压模型,左眼为实验眼,右眼为对照眼,分别于2、4、6个月后经心脏灌注内固定取材,对两侧LGN及视神经进行形态学观察;通过突触素P38单克隆抗体免疫组化技术,利用计算机图像分析,对LGN视神经末梢突触分布情况进行检测。并对两侧LGN及视神经的观察结果进行比较。结果随高眼压持续时间的延长,大鼠左眼视神经轴突数目以及右侧LGN神经元大小、密度显著减小;LGN内突触素P38免疫反应阳性产物平均光密度值呈下降趋势;LGN神经元的损伤与视神经轴突数目及突触素光密度值显著相关。结论持续性眼压升高对大鼠LGN有明显损伤作用;高眼压大鼠LGN的损伤继发于视神经的损伤。
Objective To observe the changes of cell structure of lateral geniculate nucleus (LGN) and its relationship with the loss of optic nerve fibers under continuous intraocular hypertension. Methods The model of chronic ocular hypertension was established by cauterizing the scleral surface veins in rats. The left eye was the experimental eye and the right eye was the control eye. The hearts were fixed by cardiac perfusion and fixation at 2, 4 and 6 months respectively. LGN and optic nerve morphology observation; synaptophysin P38 monoclonal antibody immunohistochemistry using computer image analysis of the LGN optic nerve endings synapses distribution were detected. And on both sides of the LGN and optic nerve observation results were compared. Results With the prolongation of IOP duration, the number of left optic nerve axons and the density and density of LGN neurons in the right eye decreased significantly. The average optical density of the P38 immunoreactive products of LGN decreased gradually. LGN Neuronal damage was significantly associated with optic nerve axon number and synaptophysin optical density. CONCLUSION: Sustained elevated intraocular pressure (IOP) can significantly damage the LGN in rats. The damage of LGN in ocular hypertension secondary to optic nerve injury.