Levy N S, Adams C K
Invest Ophthalmol. 1975 Feb;14(2):91-7.
Retinal ganglion cell protein synthesis and slow axonal protein flow have been measured in eight optic nerves from four macacus rhesus monkeys after producing ganglion cell ischemia. Comparison of the slow axonal protein flowing into the two optic nerves of the same control animal reveals a variability of up to 27 per cent. Following central retinal artery ligation, infarction of the retinal ganglion cells was reflected by a 97 per cent reduction in the radioactively labeled protein within the optic nerve. This profound reduction in labeled protein within the nerve confirmed that only ganglion cell dependent intra-axonal protein flow was being measured. Ischemia to the ganglion cell axons, with preservation of blood flow to the cell soma, was obtained in two optic nerves from different animals by severing all the posterior ciliary vessels entering about the optic nerve. Six weeks later, only a modest histologic loss of axons was present in these optic nerves. However, a profound reduction (up to 97 per cent) in labeled optic nerve protein was found at four days following intravitreal leucine injection. This is the time when the optic nerve slow axonal protein flow is dominated by the foveomacular ganglion cells. The reduction in slow axonal protein flow corresponds histologically to a preferential retrograde degeneration of the foveomacular ganglion cells, suggesting increased sensitivity of the smaller foveal axons to the induced ischemia. Electrophysiologic measurements support this conduction.
在对4只恒河猴的8条视神经造成神经节细胞缺血后，对视网膜神经节细胞蛋白合成及缓慢轴突蛋白运输进行了测量。对同一对照动物的两条视神经中流入的缓慢轴突蛋白进行比较，发现差异高达27%。视网膜中央动脉结扎后，视网膜神经节细胞梗死表现为视神经内放射性标记蛋白减少97%。神经内标记蛋白的这种显著减少证实所测量的仅为依赖神经节细胞的轴突内蛋白运输。通过切断进入视神经周围的所有睫状后血管，在来自不同动物的两条视神经中造成神经节细胞轴突缺血，而细胞体血流得以保留。六周后，这些视神经中仅出现轻微的轴突组织学损失。然而，在玻璃体内注射亮氨酸4天后，发现视神经标记蛋白显著减少（高达97%）。这正是视神经缓慢轴突蛋白运输由黄斑中心凹神经节细胞主导的时期。缓慢轴突蛋白运输的减少在组织学上对应于黄斑中心凹神经节细胞的优先逆行性变性，提示较小的黄斑轴突对诱导性缺血更为敏感。电生理测量结果支持这一传导情况。
