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Degeneration of neuronal cell bodies following axonal injury in Wld S mice
Author(s) -
Wang Ai Ling,
Yuan Ming,
Neufeld Arthur H.
Publication year - 2006
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.21075
Subject(s) - wallerian degeneration , axoplasmic transport , biology , retinal ganglion cell , axon , retinal degeneration , microbiology and biotechnology , degeneration (medical) , neuroscience , pathology , retina , medicine
The phenotype of Wld S (“slow Wallerian degeneration”) mice demonstrates prolonged survival of injured axons. However, whether the Wld S mutation delays degeneration of the neuronal cell body following axonal injury is unclear. We used a retrograde model of axonal transport failure in Wld S mice to test whether the mutant Wld S protein has any beneficial effect on the neuronal cell body. Retrograde axonal transport was physically blocked by optic nerve crush and confirmed by the absence of Fluoro‐Gold labeling in wild‐type and in Wld S mice. After this axonal injury, there was marked protection of axonal degeneration in the Wld S phenotype, as confirmed by immunohistochemistry and electron microscopy. However, the Wld S protein, localized in the nucleus of retinal ganglion cells, did not prevent or delay degeneration of the retinal ganglion cell body, confirmed by TUNEL staining and Fluoro‐Gold labeling. These results imply that, after axonal injury, Wallerian degeneration of axons and degeneration of the neuronal cell body have different mechanisms, which are autonomous and independent of each other. Although the Wld S phenotype can be used to demonstrate stable enucleate axons, the mutation is unlikely to protect neurons in neurodegenerative diseases in which there is failure of retrograde transport. © 2006 Wiley‐Liss, Inc.