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Nerve distal axon injury-induced Wallerian degeneration is significantly delayed in Wallerian degeneration slow (Wld(s)) mutant mice, although the associated mechanisms are not completely clear and the role of Wld(s) in retinal ganglion cell (RGC) body damage is not fully understood. In the present study, a Wallerian degeneration model was established in wild-type (WT) and Wld(s) mutant mice by creating mechanical injury in the optic nerves. Wallerian degeneration and RGC body collapse were observed to be significantly delayed in the Wld(s) mice. Electroretinograms (ERG) and visual evoked potentials (VEPs) in Wld(s) mice were also significantly improved at the earlier stages (one week) following injury. The retina immunohistochemistry results showed that Wld(s) mice had more ordered cells and improved inner granular cell layer arrangement compared with the WT mice. Optic nerve Luxol Fast Blue (LFB) staining showed greater axon demyelination in WT mice than in Wld(s) mice. A large number of apoptotic cells were also observed in the WT mice. The present results suggest that the Wld(s) gene may also protect the RGC body following nerve injury.

Protective role of Wallerian degeneration slow (Wlds) gene against retinal ganglion cell body damage in a Wallerian degeneration model