A systematic study of axoplasmic transport in the normal optic nerve head is essential to the understanding of the role of this process in the pathogenesis of disease of the optic nerve. Twenty-one eyes from normal adult rhesus monkeys were subjected to intravitreal injections of tritiated leucine (3H) or proline (3H). Light microscopic autoradiographs were prepared on these eyes and optic nerves six hours to 60 days after injection. The isotope that was incorporated in cytoplasmic components associated with the slow phase of axoplasmic transport (3H leucine) became concentrated in the temporal region of the optic nerve head, unevenly distributed within axons in the axonal bundles, and apparently accumulated in axons or glial cells, or both, in the lamina choroidalis and scleralis as a broad pulse of isotope moved across the optic nerve head. Several anatomic factors, including the distribution of macular fibers, increasing amounts of glial cells within the same axonal bundles as the optic nerve passed from the lamina retinalis to the lamina scleralis, and the abrupt addition of myelin sheaths to axons behind the lamina scleralis, contributed to the complex distribution of isotope in the normal optic nerve head. Glial cell labeling was especially prominent with 3H proline.
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