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首页> 外文期刊>BMC Neuroscience >Progressive ganglion cell loss and optic nerve degeneration in DBA/2J mice is variable and asymmetric
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Progressive ganglion cell loss and optic nerve degeneration in DBA/2J mice is variable and asymmetric

机译：DBA / 2J小鼠的进行性神经节细胞丢失和视神经变性是可变且不对称的

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Background Glaucoma is a chronic neurodegenerative disease of the retina, characterized by the degeneration of axons in the optic nerve and retinal ganglion cell apoptosis. DBA/2J inbred mice develop chronic hereditary glaucoma and are an important model system to study the molecular mechanisms underlying this disease and novel therapeutic interventions designed to attenuate the loss of retinal ganglion cells. Although the genetics of this disease in these mice are well characterized, the etiology of its progression, particularly with respect to retinal degeneration, is not. We have used two separate labeling techniques, post-mortem DiI labeling of axons and ganglion cell-specific expression of the βGeo reporter gene, to evaluate the time course of optic nerve degeneration and ganglion cell loss, respectively, in aging mice. Results Optic nerve degeneration, characterized by axon loss and gliosis is first apparent in mice between 8 and 9 months of age. Degeneration appears to follow a retrograde course with axons dying from their proximal ends toward the globe. Although nerve damage is typically bilateral, the progression of disease is asymmetric between the eyes of individual mice. Some nerves also exhibit focal preservation of tracts of axons generally in the nasal peripheral region. Ganglion cell loss, as a function of the loss of βGeo expression, is evident in some mice between 8 and 10 months of age and is prevalent in the majority of mice older than 10.5 months. Most eyes display a uniform loss of ganglion cells throughout the retina, but many younger mice exhibit focal loss of cells in sectors extending from the optic nerve head to the retinal periphery. Similar to what we observe in the optic nerves, ganglion cell loss is often asymmetric between the eyes of the same animal. Conclusion A comparison of the data collected from the two cohorts of mice used for this study suggests that the initial site of damage in this disease is to the axons in the optic nerve, followed by the subsequent death of the ganglion cell soma.
机译：背景技术青光眼是视网膜的一种慢性神经变性疾病，其特征是视神经轴突变性和视网膜神经节细胞凋亡。 DBA / 2J近交小鼠发展为慢性遗传性青光眼，是研究该疾病的分子机制和旨在减轻视网膜神经节细胞损失的新型治疗手段的重要模型系统。尽管在这些小鼠中该疾病的遗传学已被很好地表征，但其进展的病因学，特别是关于视网膜变性的病因学却没有。我们已经使用了两种单独的标记技术，即轴突的事后DiI标记和βGeo报告基因的神经节细胞特异性表达，以分别评估衰老小鼠的视神经变性和神经节细胞损失的时程。结果以轴突丧失和神经胶质变性为特征的视神经变性首先出现在8至9个月大的小鼠中。变性似乎遵循逆行过程，其中轴突从其近端朝向球体死亡。尽管神经损伤通常是双侧的，但疾病进展在个别小鼠的眼睛之间是不对称的。一些神经通常在鼻周边区域也表现出轴突束的局部保存。在某些8至10个月大的小鼠中，神经节细胞的丧失与βGeo表达的丧失有关，在大多数10.5个月以上的小鼠中普遍存在。大多数眼睛在整个视网膜上均显示神经节细胞的均匀丧失，但是许多年轻的小鼠在从视神经头到视网膜周围的区域内表现出细胞的局灶性丧失。与我们在视神经中观察到的相似，在同一只动物的眼睛之间神经节细胞的丢失通常是不对称的。结论从两个用于该研究的小鼠中收集的数据的比较表明，该疾病的最初损害部位是视神经轴突，随后神经节细胞体死亡。

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