Slow axonal protein transport and visual function following retinal and optic nerve ischemia.

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.