Inflammatory demyelination induces axonal injury and retinal ganglion cell apoptosis in experimental optic neuritis.

摘要: Optic neuritis is an inflammatory disease of the optic nerve that often occurs in patients with multiple sclerosis and leads to permanent visual loss mediated by retinal ganglion cell (RGC) damage. high frequency relapsing-remitting experimental autoimmune encephalomyelitis (EAE), animal model sclerosis, significant RGCs. In current study, mechanisms RGC this were examined determine whether inflammation-induced axonal injury mediates apoptotic death RGCs retrogradely labeled injection fluorogold into superior colliculi 6-7 week old female SJL/J mice. EAE was induced one later immunization proteolipid protein peptide. detected infiltration on histological examination as early 9 days after immunization, peak incidence day 12. Demyelination occurred 1-2 inflammation began. Loss axons following demyelination, occurring 13 post-immunization. Axonal prior bodies at 14. Apoptotic cells also observed 14 layer eyes neuritis, but not control eyes. Together these results suggest demyelination direct neuritis. die mechanism triggered injury. Potential neuroprotective therapies prevent from will likely need be initiated preserve neuronal function.