Abstract
Glaucoma is a complex disease affecting an estimated 70 million people worldwide, characterised by the progressive degeneration of retinal ganglion cells and accompanying visual field loss. The common site of damage to retinal ganglion cells is thought to be at the optic nerve head, however evidence from other optic neuropathies and neurodegenerative disorders suggests that dendritic structures undergo a prolonged period of atrophy that may accompany or even precede soma loss and neuronal cell death. Using the DBA/2J mouse model of glaucoma this investigation aims to elucidate the impact of increasing intraocular pressure on retinal ganglion cell dendrites using DBA/2J mice that express YFP throughout the retinal ganglion cells driven by Thy1 (DBA/2J.Thy1(YFP)) and DiOlistically labelled retinal ganglion cells in DBA/2J mice. Here we show retinal ganglion cell dendritic degeneration in DiOlistically labelled DBA/2J retinal ganglion cells but not in the DBA/2J.Thy1(YFP) retinal ganglion cells suggesting that a potential downregulation of Thy1 allows only ‘healthy’ retinal ganglion cells to express YFP. These data may highlight alternative pathways to retinal ganglion cell loss in DBA/2J glaucoma.
Highlights
Glaucoma is a complex multifactorial disease, which affects an estimated 70 million people worldwide
These have been confirmed in human glaucoma, in animals with a scleral lamina and those with a glial lamina [8,9] consistent with the hypothesis that axonal damage is the principle driver of retinal ganglion cell loss
Dendritic pruning has been reported as a consistent feature of retinal ganglion cell damage in experimental glaucoma [10,31]
Summary
Glaucoma is a complex multifactorial disease, which affects an estimated 70 million people worldwide It is characterised by the selective and progressive loss of retinal ganglion cells (RGCs) and associated reduction in visual field [1,2,3,4,5,6,7]. Several lines of experimental enquiry have confirmed that the optic nerve head is a site of early damage These have been confirmed in human glaucoma, in animals with a scleral lamina (non human primates, NHP) and those with a glial lamina [8,9] consistent with the hypothesis that axonal damage is the principle driver of retinal ganglion cell loss. There has been considerable interest in the use of animal models to study RGC degenerative events following axon trauma where dendritic atrophy has been followed with in vivo imaging in mice expressing Thy1-YFP in RGCs [13]. Given the flexibility of the mouse for genetic studies, murine models offer the greatest opportunity to determine the mechanisms underlying these degenerative changes and their relationship to axonal damage
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