Research for optic nerve damage in glaucoma

研究了实验性灵长类青光眼的轴突转运损伤及其与青光眼视神经损伤的关系。采用前房灌注法研究青光眼快速轴突转运。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。在筛板水平也显示了最小的轴突运输阻塞。结果显示，不幸的是，在常规光学显微镜下无法显示。然而，缓慢的轴突运输表明在筛板处有明显的阻塞。此外，视神经层后部分也可见轴突运输阻滞。这一结果为轴突运输损伤提供了新的信息，因为到目前为止，在急性IOP升高时，轴突运输阻塞被报道在筛层水平。我们在1994年的日本青光眼杂志上报道了这些数据。我们仍在使用暗场显微镜检查实验性青光眼的快速轴突转运异常，以显示正常眼和青光眼的明显区别。慢轴突传输数据不够令人印象深刻，因为银颗粒的颜色并非完全黑色，组织放射自显影应重复。我们一致认为，评论和乳液涂层组织现在在黑暗和寒冷的盒子里进行开发。开发时间将在5月至6月之间。所有数据将在95年8月左右完成并最终修订。

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.