This proposal concerns the pathogenesis of nerve fiber damage in glaucoma. A number of experimental and clinical studies suggest the site of nerve fiber injury in this disease is the lamina scleralis of the optic disc. Two popular theories suggest as causative compression of nerve fibers due to distortion of disc structure or ischemia of nerve fibers due to defective perfusion of the lamina. Both theories are based on the presence of a high order of retinotopy in the disc and in the nerve fiber layer near the disc. Past studies of this retinotopy produced conflicting results. We propose to examine the retinopic organization of optic nerve fibers in retina, disc, nerve, chiasm and tract to the monkey. Individual fibers will be stained by intra-axonal injection of HRP and traced in stepped serial sections. We will study a primate model of glaucoma to determine the size, origin and pathway of individual injured fibers. These studies will also provide a morphometric description of early changes in the lamina scleralis in ocular hypertension. An ancillary study will make use of the primate glaucoma model to determine the usefulness of the focal pattern ERG and pattern VER to reveal early optic nerve fiber dysfunction.
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