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and ß Retinal Ganglion Cells in Cats with Chronic Glaucoma
1From the Vision Research Laboratory, Center for Brain Science Research and State Key Laboratory of Medical Neurobiology, School of Life Sciences, Fudan University, Shanghai, China; the 2Vision Research Laboratory, Department of Neurobiology and Biophysics, School of Life Sciences, University of Science and Technology, Hefei, China; the 3Laboratory of Visual Information Processing, Institute of Biophysics, Chinese Academy of Sciences, Beijing, China; and the 4Department of Ophthalmology, Tianjin Medical University, Tianjin, China.
PURPOSE. To study changes in the dendritic morphology of retinal ganglion cells (RGCs) in cats with experimental chronic glaucoma.
METHODS. Chronic elevation of intraocular pressure (IOP) was produced by injecting endogenous ghost red blood cells into the unilateral anterior chamber of the feline eyes for 1 month. The morphologic features of retrograde-labeled RGCs by bilateral injection of horseradish peroxidase (HRP) into layers A and Aa1 of the lateral geniculate nucleus (LGN) were examined and compared between the normal and glaucomatous eyes. Nissl staining was used for measuring the change in cell density in the retina and the LGN.
RESULTS. Quantitative analysis of 720 labeled
and ß type RGCs showed that the cell density, body size, maximum dendritic field radius, total dendritic length, and number of branch bifurcations of dendrites decreased significantly in glaucomatous eyes compared with normal ones. The cell loss and shrinkage of dendrites in
type ganglion cells in the retina was more pronounced than that in ß type cells. The cell density of all kinds of cells in the retina and LGN monotonically declined with time while IOP was elevated, and cell loss was more significant in large cells than in small ones.
CONCLUSION. Progressive cell loss and dendritic damage by chronic elevation of IOP in RGCs and LGN cells are more pronounced in the Y-channel (large cells) than the X-channel (small cells) in feline glaucomatous eyes. The dendritic structure changes and corresponding physiological deficits of RGCs occur before cell death and thus may provide an opportunity for clinical treatment.
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