Abstract
The DBA/2J mouse is a commonly used animal model in glaucoma research. The eyes of DBA/2J mice show severe age-related changes that finally lead to the degeneration of retinal ganglion cells and the optic nerve. Recent electroretinogram studies identified functional deficits, which suggest that also photoreceptor cells are involved in the pathological processes occurring in the DBA/2J mouse retina. In a comparative study, we examined anatomical and molecular changes in the retinae of DBA/2J and C57BL/6 control mice with light and electron microscopy and with PCR analyses. In the retina of the DBA/2J mouse, we found a thinning of the outer plexiform layer, the first synaptic layer in the transfer of visual signals, and age-dependent and progressive degenerative structural changes at rod photoreceptor ribbon synapses. The structural ribbon changes represent a photoreceptor synaptic phenotype that has not yet been described in this animal model of secondary angle-closure glaucoma. Furthermore, genes of the classical complement cascade were upregulated in the photoreceptor cells of aging DBA/2J mice, suggesting a putative link between ribbon synapse degradation and the innate immune system.
Highlights
IntroductionThe eyes of DBA/2J mice show severe agerelated changes that include iris stroma atrophy and pigment dispersion, increase of intraocular pressure (IOP), and degenerative changes of retinal ganglion cells (RGC) and the optic nerve [1,2,3]
The DBA/2J mouse is a commonly used inbred strain for glaucoma research
Because of the reported functional deficits in the outer retina of the DBA/2J mouse [10,11], we searched for possible morphological alterations at the level of the outer plexiform layer (OPL), the first synaptic layer in the transfer of visual signals from the photoreceptor cells to their postsynaptic bipolar and horizontal cells
Summary
The eyes of DBA/2J mice show severe agerelated changes that include iris stroma atrophy and pigment dispersion, increase of intraocular pressure (IOP), and degenerative changes of retinal ganglion cells (RGC) and the optic nerve [1,2,3]. Because of these changes, the DBA/2J mouse serves as an accepted animal model of secondary angle-closure glaucoma [4], and an extensive literature exists, describing the degree and distribution of RGC degeneration and optic nerve damage in the DBA/2J mouse [2,3,5,6]. The results of these studies suggest that in addition to the degeneration of RGCs, photoreceptor cells are affected by the pathological processes occurring in the retina of DBA/2J mice
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