1981
DOI: 10.1016/0006-8993(81)90716-2
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‘Acrylamide-induced‘ neuropathy and impairment of axonal transport of proteins. II. Abnormal accumulations of smooth endoplasmic reticulum as sites of focal retention of fast transported proteins. Electron microscope radioautographic study

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Cited by 70 publications
(15 citation statements)
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“…Additional studies documented accumulations of tubulovesicular profiles within axons prior to degeneration (Abou-Donia and Lapadula, 1990), a pathology that is consistent with stagnation of membrane traffic (Chretien et al, 1981; Souyri et al, 1981). More recent work in our laboratories indicated that repeated exposures to OPs at doses that were not associated with acute signs of toxicity can lead to deficits in axonal transport.…”
Section: Op Targets Other Than Cholinesterasementioning
confidence: 85%
“…Additional studies documented accumulations of tubulovesicular profiles within axons prior to degeneration (Abou-Donia and Lapadula, 1990), a pathology that is consistent with stagnation of membrane traffic (Chretien et al, 1981; Souyri et al, 1981). More recent work in our laboratories indicated that repeated exposures to OPs at doses that were not associated with acute signs of toxicity can lead to deficits in axonal transport.…”
Section: Op Targets Other Than Cholinesterasementioning
confidence: 85%
“…This is shown by their ability to control axonal transport, to modulate neurofilaments and axon caliber, to form ASNs, and to support nerve fiber regeneration (de Waegh et al, 1992;Cole et al, 1994;Rath et al, 1995;Gatzinsky, 1996;Peles and Salzer, 2000;Martini, 2001). In diseased myelinated motor and sensory axons, such as after peripheral nerve injury or in toxically induced dying back axonopathies where the amount of organelles and membranous debris is considerably increased in the axoplasm, extensive ASNs filled with organelles are present in those parts of the axon that are in contact with intact myelinating Schwann cells, i.e., proximal to nerve segments undergoing Wallerian degeneration (Spencer and Thomas, 1974;Spencer and Schaumburg, 1978;Chretien et al, 1981;Berthold et al, 1983b). Elaborate ASNs are also a common feature in aging motor nerve fibers that show intact morphology (Thomas et al, 1980;Grover-Johnson and Spencer, 1981;King, 1994).…”
Section: Discussionmentioning
confidence: 99%
“…This hypothesis has been based on observations of static ultrastructure in old and injured axons and during pathological conditions, such as toxically induced peripheral neuropathies, in which ASNs can be very prominent and show increased contents of degenerate organelles and membranous debris (Berthold et al, 1983;Cavanagh et al, 1990;Grover-Johnson and Spencer, 1981;Singer and Steinberg, 1972;Spencer and Schaumburg, 1978;Spencer and Thomas, 1974;Thomas et al, 1980). It has also been noted that ASNs of rat and chicken PNS nerve fibres can accumulate axoplasm containing newly synthesised material as it is transported down the axon from the perikaryon (Chretien et al, 1981;Spencer and Griffin, 1982), and we have previously reported that the number of lysosomes in some paranodal ASN regions of cat alpha-motor axons increases if there is an increase in the amount of lysosomes in the main axoplasm (Gatzinsky and Berthold, 1990). The present study now provides direct evidence that exogenous material in association with organelles that are transported toward the motor neuron perikaryon from distal axon parts can be sequestered within paranodal ASNs situated far away from the site of tracer administration.…”
Section: Discussionmentioning
confidence: 99%