{'fraction_non_alphanumeric': 0.021216407355021217, 'fraction_numerical': 0.002828854314002829, 'mean_word_length': 5.431818181818182, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Degeneration of neuronal cell bodies following axonal injury in WldS mice

The phenotype of WldS (“slow Wallerian degeneration”) mice demonstrates prolonged survival of injured axons. However, whether the WldS mutation delays degeneration of the neuronal cell body following axonal injury is unclear. We used a retrograde model of axonal transport failure in WldS mice to test whether the mutant WldS 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 WldS mice. After this axonal injury, there was marked protection of axonal degeneration in the WldS phenotype, as confirmed by immunohistochemistry and electron microscopy. However, the WldS 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 WldS 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.