{'fraction_non_alphanumeric': 0.03502626970227671, 'fraction_numerical': 0.023642732049036778, 'mean_word_length': 4.953125, 'pattern_counts': {'":': 0, '<': 1, '<?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}}
Retardation of fast axonal transport in wobbler mice

To investigate axonal function in a model of early motor neuron disease, we examined fast and slow components of anterograde axonal transport in the less‐affected hindlimb motor neurons of wobbler mice. To study the fast component (FC), we injected tritiated amino acids into the lumbar spinal cord and retrieved the sciatic nerve after 2 or 3 h. The transport distance was the extent of the plateau of labeling; regression analysis indicated that FC was 25% slower in wobbler mice than in unaffected littermates (P < 0.01). To study slow component (SC), [35S] methionine was injected. Transport distances were to the peaks of labeling for structural proteins after 2 or 3 weeks. Rates for each subcomponent (SCa and SCb) were unaffected by wobbler disease. Because the rate of retrograde FC is also unaffected (Mitsumoto et al., Muscle & Nerve 13:121–126, 1990), we conclude that wobbler disease specifically retards anterograde FC in less‐affected hindlimb motor neurons, whereas all components of axonal transport are retarded in forelimb motor neurons. © 1993 John Wiley & Soncs, Inc.