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Updated: Aug 23, 2026
In Vivo Dynamics of Retinal Microglial Activation During Neurodegeneration: Confocal Ophthalmoscopic Imaging and Cell Morphometry in Mouse Glaucoma
Published on: May 11, 2015
Differential dendritic shrinkage of alpha and beta retinal ganglion cells in cats with chronic glaucoma
Tiande Shou1, Jie Liu, Wei Wang
1Vision Research Laboratory, Center for Brain Science Research and State Key Laboratory of Medical Neurobiology, School of Life Sciences, Fudan University, Shanghai, China. tdshou@fudan.edu.cn
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 alpha and beta 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 alpha type ganglion cells in the retina was more pronounced than that in beta 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.
