Fast Axonal Transport: a Site of Acrylamide Neurotoxicity: a Rebuttal

Alternative viewpoints to our hypothesis are offered in the accompanying critiques. There appears to be a general consensus that acrylamide compromises fast axonal transport. This represents advancement in our thinking since the myriad of apparently contradictory experimental results have been resol...

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Bibliographic Details
Published in:Neurotoxicology (Park Forest South) 2002-07, Vol.23 (2), p.265-270
Main Authors: Sickles, Dale W, Stone, Derek, Friedman, Marvin
Format: Article
Language:English
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Summary:Alternative viewpoints to our hypothesis are offered in the accompanying critiques. There appears to be a general consensus that acrylamide compromises fast axonal transport. This represents advancement in our thinking since the myriad of apparently contradictory experimental results have been resolved by identification of the differences in experimental designs that contributed to the variability. Both respondents recognize kinesin, the anterograde motor protein, as a site of action in producing fast anterograde axonal transport (faAXT) reductions. Sabri and Spencer present data supporting additional sites of acrylamide action. The most controversial component of our hypothesis is whether the faAXT reductions are related to the development of behavioral changes characteristic of acrylamide neurotoxicity. The void of information regarding this issue must be addressed to adequately assess the contribution of faAXT compromise to axon (including the axon terminals) functionality.
ISSN:0161-813X
1872-9711
DOI:10.1016/S0161-813X(02)00026-8