Research for optic nerve damage in glaucoma

我们研究了实验性灵长类青光眼的轴突运输损伤及其与青光眼视神经损伤的关系。用前房插管的方法研究了青光眼的快速轴突运输。由于视网膜神经节细胞的丢失，实验眼的轴突运输量显著减少。筛板水平轴突运输受阻程度最小。不幸的是，结果显示在常规光学显微镜下显示太少。然而，缓慢的轴突运输在筛板显示明显的阻塞。此外，这种轴突运输障碍甚至在视神经的板层后部分也可见。这一结果增加了有关轴突运输损伤的新信息，因为到目前为止，据报道，在急性眼压升高的情况下，轴突运输受阻于筛板水平。我们向日本青光眼杂志1994报告了这一数据。我们仍在使用暗视野显微镜检查实验性青光眼的快速轴突运输异常，以显示正常眼和青光眼之间的明显差异。缓慢的轴突运输数据不够令人印象深刻，因为银粒的颜色并不完全是黑色的，组织放射自显影应该重复。我们同意，评论和乳胶涂层组织现在处于黑暗和冷箱中，有待开发。开发时间将在5月至6月之间。所有数据将于95年8月左右完成最终修订。

We studied the axonal transport damage in experimentally induced primate glaucoma and its relation to glaucomatous optic nerve injury.Fast axonal transport was studied in glaucomatous eyes using the canulation method to the anterior chamber. The amount of axonal transport was reduced dramatically in experimental eyes due to the loss of retinal ganglion cells. Also showed the minimum axonal transport blockage at the level of lamina cribrosa. The results demonstrated unfortunately too miumum to show up under routine light microscope.Slow axonal transport, however, demonstrated clear blockage at the lamina cribrosa. Furthrmore, such axonal transport blockage was seen even retro-laminar portion of optic nerve. The result add new information about axonal transport damage, since so far axonal transport blockage was reported to be seen at the level of lamina cribrosa in acute IOP elevation.We reported the data to the Japanese Glaucoma journal 1994.We are still examining the fast axonal transport abnormality in experimental glaucoma using the dark field microscopy to show the clear difference between normal and glaucomatous eyes.Slow axonal transport data was not impressive enough since the color of silver grains are not totally black and tissue autoradiography should be repeated.We agreed that comment and emulsion coated tissue are now in the dark and cold box for development. The time to be developed will be between May and June. The all data will be completed around August 95' for final revision.