P3

Source and influence of calcium entry in retinal ganglion cells during the preclinical phase of autoimmune optic neuritis

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The figure above shows calcium entry pathways under physiological and inflammatory conditions. Proposed calcium channels and pumps responsible for elevated internal calcium under inflammatory conditions in both neuronal soma and axons, with potential downstream signalling pathways leading to neuronal cell death.

Project 3 concentrates on calcium dynamics and calcium channel dysfunction during the phase of preclinical RGC degeneration in autoimmune optic neuritis/experimental autoimmune encephalomyelitis.
Retinal gangion cell degeneration had recently been detected to occur prior to inflammatory infiltration and demyelination of the optic nerves, which is unexpected given the presumed inflammatory nature of the disease and the fact that the retina is free of myelin.