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Abstract #5563 Published in IGR 2-1
Chronology of optic nerve head and retinal responses to elevated intraocular pressure (see comments)
Johnson EC; Deppmeier LM; Wentzien SK; Hsu I; Morrison JCInvestigative Ophthalmology and Visual Science 2000; 41:431-442
PURPOSE: To determine the chronology of optic nerve head and retinal responses to elevated intraocular pressure (IOP). METHODS: After one to 39 days of unilaterally elevated IOP, experimental and fellow rat eyes were examined for morphology and immunohistochemical labelling alterations and for ganglion cell DNA fragmentation. RESULTS: Mean IOP for the experimental eyes was 36±8 mmHg, an approximately 15-mmHg elevation above normal values. By seven days of pressure elevation above 40 mmHg, endogenous immunostaining for brain-derived neurotrophic factor and neurotrophin 4/5 was absent from the nerve head and superior retina, whereas normal labelling was present in the inferior retina and distal optic nerve of these same eyes. These changes were preceded by a loss of gap junctional connexin43 labelling and astrocytic proliferation in the nerve head and by increased retinal ganglion cell layer apoptosis in the retina. Nerve head depletion of neurotrophins coincided with evidence of axonal degeneration, loss of astrocytic glial fibrillary acidic protein staining, and spread of collagen VI vascular immunolabelling. After longer durations at these same pressures, neurotrophin labelling returned to nerve head glia and scattered retinal ganglion cells. CONCLUSIONS: Optic nerve head and retinal responses, including the depletion of endogenous neurotrophins, are readily identified in the rat eye after experimental IOP elevation. However, the apparent chronology of these responses suggests that the withdrawal of neurotrophic support was not the only determinant of retinal ganglion cell apoptosis and axonal degeneration in response to pressure.
Dr. E.C. Johnson, Kenneth C. Swan Ocular Neurobiology Laboratory, Casey Eye Institute, Portland, OR 97201, USA johnsoel@ohsu.edu
Classification:
1.3 Pathogenesis (Part of: 1 General aspects)
5 Experimental glaucoma; animal models
