Tuesday, June 20, 2017

Regenerating optic pathways

Less than a mile down Embarcadero Road from Newell Road is Stanford University's Ophthalmology department. In Science Vol. 356, Issue 6342, pp. 1031–1034, three researchers from the School of Medicine report on the current status in retinal ganglion cell (RGC, pink in the figure) regeneration. When the optic nerve is severed, for example after an accident or with glaucoma, the retinal ganglion cells quickly die off. Even if the rest of the retina remains intact, sight is lost.

The retinal ganglion cells are part of the central nervous system, thus unlike in the peripheral nervous system, severed axons do not regenerate. After injury and inflammation, in the eye, there is a balance of activating and inhibiting factors. For example, amacrine cells (orange in the figure) release zinc, which is an inhibitor, while the lens can cause macrophages to release oncomodulin, a protein that promotes RGC axon extension. The challenge is to understand these balancing mechanisms. A further challenge is to regrow the axons correctly all the way to the lateral geniculate nucleus (LGN).

The authors outline three possible avenues for restoring the RGCs and thus sight.

retinal ganglion and amacrine cells in the retina

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