Progressive Deficits in Retrograde Axon Transport Precede Degeneration of Motor Axons in Acrylamide Neuropathy
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1988/02/02
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Description:Single injection of acrylamide (1.3 mmol/kg, i.p.) inhibited retrograde axon transport of [125I]tetanus toxin in hen sensory and motor axons. Retrograde axon transport deficits appeared within hours of dosing with acrylamide. The inhibitory effect of acrylamide on retrograde axon transport was transient since transport deficits were not detectable 35 h after dosing. Acrylamide impaired the retrograde movement but not the uptake of [125I]tetanus toxin in the axon. Multiple doses of acrylamide (0.42 mmol/kg, i.p.) induced progressive clinical signs of acrylamide neuropathy that correlated with increasing deficits in retrograde axon transport of [125I]tetanus skin to ventral spinal cord. Deficits were also observed in sensory neurons but were not statistically significant. Accumulated decrements in retrograde axon transport may be the underlying cause of degeneration of motor axons in acrylamide neuropathy in fowl. [Description provided by NIOSH]
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ISSN:0006-8993
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Pages in Document:18-24
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Volume:440
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Issue:1
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NIOSHTIC Number:nn:20060128
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Citation:Brain Res 1988 Feb; 440(1):18-24
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Contact Point Address:M.I. Sabri. Institute of Neurotoxicology, Albert Einstein College of Medicine, Kennedy Center, Room 518, Bronx, NY 10461, U.S.A.
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CAS Registry Number:
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Federal Fiscal Year:1988
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Performing Organization:Yeshiva University, New York, New York
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Peer Reviewed:True
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Start Date:19850501
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Source Full Name:Brain Research
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End Date:19910430
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Main Document Checksum:urn:sha-512:b09b7b3ff93d2286031c0d553051a6981ac0eeca0cdbdd31b5fb2eba0afd9b4166e403a21a920df5eaa02031f1ca466e704b27af068f197ffd0074b558767036
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