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Published 24 October 2005. doi:10.1083/jcb.200506099
The Rockefeller University Press, 0021-9525 $8.00
JCB, Volume 171, Number 2, 313-325
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Article

 Retinal ganglion cell degeneration is topological but not cell type specific in DBA/2J mice

Tatjana C. Jakobs1, Richard T. Libby2, Yixin Ben1, Simon W.M. John2, and Richard H. Masland1

1 Howard Hughes Medical Institute, Harvard Medical School, Boston, MA 02114
2 Howard Hughes Medical Institute, The Jackson Laboratory, Bar Harbor, ME 04609

Correspondence to Richard H. Masland: masland{at}helix.mgh.harvard.edu

Using a variety of double and triple labeling techniques, we have reevaluated the death of retinal neurons in a mouse model of hereditary glaucoma. Cell-specific markers and total neuron counts revealed no cell loss in any retinal neurons other than the ganglion cells. Within the limits of our ability to define cell types, no group of ganglion cells was especially vulnerable or resistant to degeneration. Retrograde labeling and neurofilament staining showed that axonal atrophy, dendritic remodeling, and somal shrinkage (at least of the largest cell types) precedes ganglion cell death in this glaucoma model. Regions of cell death or survival radiated from the optic nerve head in fan-shaped sectors. Collectively, the data suggest axon damage at the optic nerve head as an early lesion, and damage to axon bundles would cause this pattern of degeneration. However, the architecture of the mouse eye seems to preclude a commonly postulated source of mechanical damage within the nerve head.

Abbreviations used in this paper: ChAT, choline acetyltransferase; GABA, {gamma}-aminobutyric acid; GCL, ganglion cell layer; INL, inner nuclear layer; IPL, inner plexiform layer; NOS, nitric oxide synthase; TH, tyrosine hydroxylase.


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