Axoplasmic Flow in Axonal Neuropathies I. Axoplasmic Flow in Cats With Toxic Neuropathies

Bradley, Walter G.; Williams, M. H.

doi:10.1093/brain/96.2.235

Cited by 82 publications

(12 citation statements)

References 29 publications

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“…The present study of slow and fast anterograde axonal transport of labelled proteins in acrylamide intoxicated rats has shown that the slow transport velocity is normal in animals with severe motor incoordination, as well as in those with only mild signs of neuropathy. In accordance with this finding, a normal transport velocity was reported by Bradley and Williams (1973) and by Sumner et al (1976) from studies on sciatic sensory nerves of cats with acrylamide neuropathy.…”

Section: Discussionsupporting

confidence: 81%

“…It is a new observation of the present study that a decreased fractional amount of protein label is carried in SCa of severely disabled animals. This finding possibly explains the almost historic controversy between the study of Pleasure et al (1969) and that by Bradley and Williams (1973). In the former study a decreased amount of activity was found by autoradiography of cat sensory and motor roots a few days after labelling, whereas the latter study showed SC profiles moving at a normal velocity in sensory fibres of the same model.…”

Section: Discussionmentioning

confidence: 83%

See 1 more Smart Citation

Anterograde Axonal Transport in Rats During Intoxication with Acrylamide

Sidenius

Jakobsen

1983

Journal of Neurochemistry

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Anterograde axonal transport was examined in sensory nerves of rats intoxicated with a low dose (group I) or a high dose (group II) of acrylamide. After injection of either [35S]methionine and [3H]fucose or [3H]proline into the dorsal root ganglia of the 5th lumbar roots, distribution of protein label was measured in 3‐mm segments of the sciatic nerve at intervals of 2 h, 4 h, 10 days, and 26 days. No difference in ganglion incorporation was present at 4 h, and the fast transport velocity of methionine label also remained normal [14.7 ± 1.3 mm/h (mean ± SD) in controls versus 14.6 ± 0.3 mm/h and 15.4 ± 1.2 mm/h in acrylamide group I and II, respectively]. Neither was there any decrease in transport velocity of proline label of slow component b (4.18 ± 0.29 mm/day in controls versus 4.29 ± 0.17 mm/d and 4.22 ± 0.29 mm/day in acrylamide group I and II, respectively). In slow component a, however, a significant reduction in the fractional amount of proline label was found (20.8 ± 4.0% in controls versus 17.6 ± 14.9% and 9.7 ± 5.9% in acrylamide group I and II, respectively). Again no decrease in transport velocity was observed (1.03 ± 0.02 mm/day in controls versus 1.06 ± 0.08 mm/day and 1.07 ± 0.03 mm/day in acrylamide group I and II, respectively), and closer inspection of the activity along the nerve did not reveal any alteration in skewness or ‘peakedness’ of the distribution curve. The reduction in amount of protein carried in the slow axonal transport component in rats with severe acrylamide neuropathy (group II) could be associated with fibre breakdown at a late stage of the neuropathic process. The most important consequence of the study is, however, that in contrast to previous suggestions, during acrylamide intoxication no changes are present in protein incorporation or in anterograde axonal transport which can explain the initial pathological or functional abnormalities of the distal axons.

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Section: Discussionsupporting

confidence: 81%

Section: Discussionmentioning

confidence: 83%

Anterograde Axonal Transport in Rats During Intoxication with Acrylamide

Sidenius

Jakobsen

1983

Journal of Neurochemistry

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“…However, Bradley and Williams [34] found no diminution in slow axonal transport in acrylamidetreated animals. They did find a decrease in the velocity of the crest of fast axoplasmic transport but did not believe that this reduction was responsible for distal degeneration.…”

Section: Discussionmentioning

confidence: 91%

Giant axonal neuropathy: A childhood disorder of microfilaments

Koch

Schultz

Williams

et al. 1977

Annals of Neurology

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A sural nerve biopsy was performed on an 8-year-old boy with a chronic, slowly progressive polyneuropathy. Light and electron microscopy as well as teased nerve-fiber preparations demonstrated numerous giant axons filled with closely packed neurofilaments. Both myelinated and unmyelinated fibers were involved. Segmental demyelination, remyelination, and onion-bulb formation by multiple Schwann cell processes were observed, suggesting recurrent Schwann cell dysfunction. Abundant aggregates of cytoplasmic microfilaments occurred in Schwann cells, endothelial cells, perineurial cells, endoneurial fibroblasts, and endomysial fibroblasts. These findings support the proposal that giant axonal neuropathy is a generalized disorder of cytoplasmic microfilaments and that segmental demyelination occurs concomitantly with axonal and Schwann cell disease. The pathogenesis of this rare disorder is discussed with reference to experimental toxic neuropathies.

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“…This leads to a depletion in the amount of material reaching the distal regions of axons where degeneration begins (36,38). Another hypothesis suggests that acrylamide inactivates the axonal transport system by which substances, assembled in the neuron cell body, are transported along the axon (39,40). Finally, it has been suggested that if acrylamide inactivated a substance in the axon, which is dependent for its supply on the nerve cell body, this alone could account for the dying-back process (7,27,28).…”

Section: Site Of Neurotoxic Actionmentioning

confidence: 99%