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Abstract #5961 Published in IGR 2-2
Optic nerve head structure in glaucoma: astrocytes as mediators of axonal damage
Morgan JEEye 2000; 14: 437-444
Increased intraocular pressure (IOP) is recognized as the principal risk factor for the development of glaucomatous cupping of the optic disc. The hypothesis that it disrupts the function of retinal ganglion cell axons by increasing mechanical forces on the lamina cribrosa of the optic nerve head has received considerable experimental support. However, many patients with glaucoma will have progressive cupping even though the IOPs remain within the normal range, suggesting that mechanical compression is unlikely to be the sole cause of optic nerve damage. Clinical studies have emphasized the role of other factors, such as optic nerve head ischemia, in generating optic disc cupping. One of the outstanding problems in understanding optic nerve head dysfunction in glaucoma has been the elucidation of the pathways that could integrate the effects of IOP and ischaemia to generate the characteristic changes seen. This review considers the role that optic nerve head astrocytes might play in the initiation of axon damage, based on the hypothesis that these cells are sensitive to mechanical or ischemic factors and are important for the maintenance of retinal ganglion physiology. It discusses their role in the remodelling of the structure of the lamina cribrosa and the effect that this might have on axon function. Recent evidence has shown that the modulation of astrocyte activity, for example, by the reduction of the production of nitric oxide, may prevent retinal ganglion cell death in ocular hypertension. The possibility that astrocyte-axon interactions are important in the development of glaucomatous optic neuropathy suggests new avenues of therapeutic intervention, not related to the control of IOP, that would prevent retinal ganglion cell death in glaucoma.
Dr. J.E. Morgan, Department of Ophthalmology, University Hospital of Wales, Heath Park, Cardiff CF4 4XW, UK
Classification:
1.3 Pathogenesis (Part of: 1 General aspects)
