Lens Injury Stimulates Axon Regeneration in the Mature Rat Optic Nerve

In mature mammals, retinal ganglion cells (RGCs) are unable to regenerate their axons after optic nerve injury, and they soon undergo apoptotic cell death. However, a small puncture wound to the lens enhances RGC survival and enables these cells to regenerate their axons into the normally inhibitory...

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Bibliographic Details
Published in:The Journal of neuroscience 2000-06, Vol.20 (12), p.4615-4626
Main Authors: Leon, Steven, Yin, Yuqin, Nguyen, Jennifer, Irwin, Nina, Benowitz, Larry I
Format: Article
Language:English
Subjects:
Animals
Astrocytes - physiology
Axons - physiology
Axons - ultrastructure
Cell Survival
GAP-43 Protein - analysis
Lens, Crystalline - injuries
Macrophage Activation
Macrophages - physiology
Male
Nerve Regeneration - physiology
Optic Nerve - cytology
Optic Nerve - physiology
Rats
Rats, Inbred F344
Retinal Ganglion Cells - cytology
Retinal Ganglion Cells - physiology
Time Factors
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Summary:In mature mammals, retinal ganglion cells (RGCs) are unable to regenerate their axons after optic nerve injury, and they soon undergo apoptotic cell death. However, a small puncture wound to the lens enhances RGC survival and enables these cells to regenerate their axons into the normally inhibitory environment of the optic nerve. Even when the optic nerve is intact, lens injury stimulates macrophage infiltration into the eye, Müller cell activation, and increased GAP-43 expression in ganglion cells across the entire retina. In contrast, axotomy, either alone or combined with intraocular injections that do not infringe on the lens, causes only a minimal change in GAP-43 expression in RGCs and a minimal activation of the other cell types. Combining nerve injury with lens puncture leads to an eightfold increase in RGC survival and a 100-fold increase in the number of axons regenerating beyond the crush site. Macrophage activation appears to play a key role, because intraocular injections of Zymosan, a yeast cell wall preparation, stimulated monocytes in the absence of lens injury and induced RGCs to regenerate their axons into the distal optic nerve.
ISSN:0270-6474
1529-2401
DOI:10.1523/jneurosci.20-12-04615.2000