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

Abstract 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 optimized by injecting a myelin oligodendrocyte glycoprotein (MOG 35–55 ). 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 MOG 35–55 . 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 0.0891 μm, compared with 0.1678 μm of the control group ( p  = 0.0003). The ON was strongly affected with reactive gliosis, increased axonal damage and decreased density axonal (control group 0.38038 axons/μm 2 versus EAE group 0.16 axons/μm 2 , p  = 0.00032). Conclusions In this work an animal model of EAE has been characterized 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.