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Retinal degeneration in the nervous mutant mouse. IV. Inner retinal changes
J C Ren1, E B Stubbs, M T Matthes
1Program in Neuroscience, Stritch School of Medicine, Loyola University Chicago, Maywood, IL 60153, USA.
Experimental Eye Research
|February 22, 2001
Summary
The nervous (nr/nr) mouse model shows thinning of the inner nuclear layer (INL) and inner plexiform layer (IPL) due to amacrine cell loss. Photoreceptor degeneration in these mice occurs via apoptosis.
Area of Science:
- Neuroscience
- Ophthalmology
- Genetics
Background:
- The nervous (nr/nr) mouse model is known to exhibit cerebellar Purkinje cell and retinal photoreceptor loss.
- Previous observations indicated thinner inner nuclear layer (INL) and inner plexiform layer (IPL) in nr/nr mice compared to controls.
Purpose of the Study:
- To investigate the anatomical basis of inner retinal changes in the nr/nr mouse model.
- To determine the specific cell types affected within the inner retina and the mechanism of photoreceptor degeneration.
Main Methods:
- Comparative anatomical studies of nr/nr mice and control littermates at different postnatal days (P13 and P30).
- Immunohistochemical staining using antibodies against GABA and glycine to identify specific cell populations.
- Analysis of photoreceptor cell death pathways.
Main Results:
- Significant thinning of the INL and IPL was observed in nr/nr mice by P30, but not at P13.
- A reduction in the density of GABAergic and glycinergic amacrine cells within the INL was detected.
- Photoreceptor degeneration in nr/nr mice was confirmed to proceed through an apoptotic pathway.
Conclusions:
- The nervous defect (nr/nr) leads to the degeneration of specific amacrine cell populations in the inner retina.
- These findings expand the known phenotype of the nr/nr mouse to include amacrine cell loss, in addition to photoreceptor and Purkinje cell degeneration.
- Photoreceptor death in this model is mediated by apoptosis.