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Experimental autoimmune encephalomyelitis (EAE) is a commonly used animal model of the human neurological disorder multiple sclerosis. The purpose of the present study was to investigate the effect of combined treatment with two nucleoside analogs, ribavirin and tiazofurin, on development of EAE actively induced in highly susceptible dark agouti rats. The obtained results showed that ribavirin and tiazofurin applied either separately or in combination from the onset of the firstsymptoms of EAE after its induction (therapeutic treatment) significantly suppressed EAE’s clinical symptoms. However, the most pronounced effect was gained with combined treatment, probably as a result of synergistic/additive action

INTRODUCTION 2.1. Multiple sclerosis -pathological features and pathogenesis 2.2. General mechanisms of injury and repair in MS 2.3. Patterns of demyelination in MS 2.4. Axonal damage in MS 2.5. Myelin oligodendrocyte glycoprotein (MOG) -induced experimental autoimmune encephalomyelitis (EAE) 2.6. Voltage dependent calcium channels -structure, function, distribution and classification (VDCC) 2.7. VDCCs as therapeutic targets 2.8. Magnetic resonance imaging (MRI) for visualization of MS and EAE pathology 2.9. Manganese enhanced MRI AIM OF THE STUDY 3 METHODS 3.1. Animals 3.2. Immunogen 3.3. Induction and evaluation of EAE 3.4. Retrograde labeling of RGCs 3.5. Quantification of RGC density 3.6. Optic nerve histopathology 3.7. Immunohistochemistry 3.8. Experimental setup for manganese enhanced MRI 3.9. Analysis of MR images 3.10. Labeling of the optic nerve with a calcium sensitive dye 3.11. In vivo calcium imaging 3.12. Intracerebroventricular infusion 3.13. Statistical analysis 4 RESULTS 4.1. In optic neuritis signal intensity in T1-weighted MR images is reduced and Mn 2+ -induced enhancement is prominent 4.2. High voltage-activated calcium channels mediate Mn 2+ -induced enhancement 4.3. Mn 2+ enters the inflamed ON via N-type VDCCs 4.4. N-type VDCC expression is up-regulated in optic neuritis and correlates with demyelination pattern 4.5. N-type VDCC expression correlates with immunoreactivity for β-amyloid precursor protein

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