Abstract
Optic neuritis (ON) is an early syndrome present in patients with multiple sclerosis (MS). It is defined as an autoimmune demyelinating disorder that results in axonal loss and visual disturbances. In order to characterize axonal changes during ON, we used an animal model of MS, myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE) in brown Norway rats. In this model, retinal ganglion cell (RGC) body loss is visible before inflammation of the optic nerve, suggesting that insult to the RGC body might be a primary event that triggers axonal stress, independent of later axonal loss resulting from inflammatory demyelination.
Published Version
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