Blocking Zinc Stimulates Optic Nerve Regeneration (IMAGE)
Caption
Top row: Cross-sections through the mouse retina show very little free zinc (Zn2+) in normal mice (purple staining, left panel), but high levels after the optic nerve is injured (right panel). Within an hour after nerve injury, zinc begins to accumulate in the layer of the retina where interneurons known as amacrine cells connect with the retinal ganglion cells (RGCs). Over the next two days, the zinc transfers to the RGCs themselves, causing these neurons to die and preventing them from regenerating the axons (nerve fibers) that were damaged by the injury.
Second row: Blocking the accumulation of zinc (Zn2+) with chelating compounds enables many damaged retinal ganglion cells (RGCs) to survive for months after the optic nerve is injured. The panels show healthy RGCs in the normal retina (left), in an injured, untreated retina two weeks after optic nerve injury (center) and in a treated retina two weeks after injury (right).
Bottom two panels show the optic nerve two weeks after injury at the sites denoted by the asterisks. Without treatment (upper panel), no axons regenerate beyond the injury site; treatment with a zinc chelator (bottom panel) leads to extensive axon regeneration.
Credit
Boston Children's Hospital
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