Morphology of single ganglion cells in the glaucomatous primate retina.

Kaufman Lab // Publications // Nov 06 1998

PubMed ID: 9804139

Author(s): Weber AJ, Kaufman PL, Hubbard WC. Morphology of single ganglion cells in the glaucomatous primate retina. Invest Ophthalmol Vis Sci. 1998 Nov;39(12):2304-20.

Journal: Investigative Ophthalmology & Visual Science, Volume 39, Issue 12, Nov 1998

PURPOSE To examine the degenerative effects that prolonged elevation of intraocular pressure (IOP), a risk factor commonly associated with glaucoma, has on the morphology of single ganglion cells in the primate retina.

METHODS The monkey model of glaucoma was combined with intracellular staining techniques using an isolated retina preparation. Midget and parasol cells from normal and glaucomatous eyes were labeled intracellularly, and their axons, somas, and dendritic fields were compared using confocal microscopy.

RESULTS In midget and parasol cells, the earliest signs of pressure-induced degeneration involved structural abnormalities associated with the dendritic arbor. Reductions in axon thickness appeared later, with changes in soma size occurring concomitantly or slightly later. Chronic elevation of IOP resulted in a significant decrease in the mean soma sizes of midget and parasol cells, but only parasol cells showed a significant reduction in dendritic field size and axon diameter. Comparisons of eyes with different levels of optic nerve damage, based on cup- disc ratio, showed that the axons and dendritic fields of parasol cells were significantly smaller at lower cup-disc ratios than were those of midget cells, suggesting a possible differential effect.

CONCLUSIONS In glaucoma, retinal ganglion cells undergo a pattern of degeneration that originates with the dendritic arbor and ends with shrinkage of the cell soma. Although this pattern of degeneration implies early functional deficits and retinal ganglion cell atrophy that occurs earlier than previously thought, based on ganglion cell loss alone, it also suggests a window of opportunity for effective neuroprotection.