Development and optimisation of an animal model for the study of ganglion cells in degenerative diseases of the retina and optic nerve.

INTRODUCTION

Multiple sclerosis is an autoimmune, chronic and inflammatory disease of the central nervous system with axonal demyelination, gliosis and neurodegeneration. It is considered a frequent cause of neurological disability in young adults. In this work, an Experimental Autoimmune Encephalomyelitis (EAE) model was optimised by injecting a myelin oligodendrocyte glycoprotein (MOG35-55). The ophthalmological effects were studied, as well as its use as an experimental model in other studies of retinal ganglion cell degeneration (RGC) and optic nerve (ON).

MATERIAL AND

METHODS

The study included 16 mice of 10 weeks that were placed into 2 study groups: a control group of 10 animals and another group of 6 animals with EAE that were injected with MOG35-55. The animals of the EAE model were monitored using motor disability scales. The retinas and optic nerves were processed for morphological examination by optical microscopy and ultrastructure studies.

RESULTS

The animal models presented with motor symptoms of spinal cord injury, with the first symptoms appearing between the 7th and 19th day post-injection, with a maximum disability mean of 3.5 points. In the retina, the mean RGC in the EAE group was 0.0891μm, compared with 0.1678μm of the control group (p=.0003). The ON was strongly affected with reactive gliosis, increased axonal damage and decreased density axonal (control group 0.38038 axons/μm2 versus EAE group 0.16 axons/μm2, p=.00032).

CONCLUSIONS

In this work an animal model of EAE has been characterised and detailed for the study of demyelinating alterations in the retina and the ON. Its characteristics make it an excellent tool for the study of neurodegenerative ophthalmic diseases.