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M. Yuan, A.–L. Wang, A.H. Neufeld; The Slow Wallerian Degeneration Gene, WldS, Does Not Inhibit Retrograde Retinal Ganglion Cell Death After Optic Nerve Crush . Invest. Ophthalmol. Vis. Sci. 2006;47(13):1262.
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© ARVO (1962-2015); The Authors (2016-present)
The WldS mouse is a spontaneous mutant with the phenotype of prolonged survival of injured axons ("slow Wallerian degeneration"). Much of the previous research effort has been focused on distal stumps of damaged axons. The WldS protein has been localized to the neuronal cell body. Previous work on whether the WldS mutant prolongs the survival of the cell body has been equivocal. We hypothesized that retrograde degeneration of the retinal ganglion cell bodies after optic nerve crush in WldS mice might be much slower than that in wild–type mice.
In mice, 7–8 weeks of age, the left optic nerve was crushed with forceps; the right eye served as the control At 1, 2, 4, 6 and 10 days after the crush, TUNEL–positive cells in the retinal ganglion cell layer were quantified in both WldS and wild–type mice. At 3, 7 and 14 days after the crush, the cells positive for Fluoro–Gold, a retrograde tracer, were counted to determine whether the protective effect of WldS protein on the ganglion cell bodies after optic nerve crush is the same or different, comparing WldS and wild–type mice.
Maximal TUNEL–positive cells occurred at 4 and 6 days after crush in both WldS and wild–type mice and were not significantly different. The loss of Fluoro–Gold containing retinal ganglion cell bodies at 3 and 7 days after crush were not significantly different in WldS and wild–type mice.
Retrograde degeneration of the retinal ganglion cell bodies after optic nerve crush was not significantly slower in WldS mice than that in wild–type mice. These results demonstrated that WldS protein in the retinal ganglion cell bodies does not prevent degeneration of the ganglion cell body after optic nerve crush.
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