‘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

Chrétien, M; Patey, Gilles; Souyri, F.; Droz, Bernard

doi:10.1016/0006-8993(81)90716-2

Cited by 70 publications

(15 citation statements)

References 30 publications

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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%

Functional consequences of repeated organophosphate exposure: Potential non-cholinergic mechanisms

Terry

2012

Pharmacology & Therapeutics

213

164

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The class of chemicals known as the “organophosphates” (OPs) comprises many of the most common agricultural and commercial pesticides that are used worldwide as well as the highly toxic chemical warfare agents. The mechanism of the acute toxicity of OPs in both target and non-target organisms is primarily attributed to inhibitory actions on various forms of cholinesterase leading to excessive peripheral and central cholinergic activity. However, there is now substantial evidence that this canonical (cholinesterase-based) mechanism cannot alone account for the wide-variety of adverse consequences of OP exposure that have been described, especially those associated with repeated exposures to levels that produce no overt signs of acute toxicity. This type of exposure has been associated with prolonged impairments in attention, memory, and other domains of cognition, as well as chronic illnesses where these symptoms are manifested (e.g., Gulf War Illness, Alzheimer’s disease). Due to their highly reactive nature, it is not surprising that OPs might alter the function of a number of enzymes and proteins (in addition to cholinesterase). However, the wide variety of long-term neuropsychiatric symptoms that have been associated with OPs suggests that some basic or fundamental neuronal process was adversely affected during the exposure period. The purpose of this review is to discuss several non-cholinesterase targets of OPs that might affect such fundamental processes and includes cytoskeletal and motor proteins involved in axonal transport, neurotrophins and their receptors, and mitochondria (especially their morphology and movement in axons). Potential therapeutic implications of these OP interactions are also discussed.

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Section: Op Targets Other Than Cholinesterasementioning

confidence: 85%

Functional consequences of repeated organophosphate exposure: Potential non-cholinergic mechanisms

Terry

2012

Pharmacology & Therapeutics

213

164

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“…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%

Early onset of degenerative changes at nodes of Ranvier in alpha‐motor axons of Cntf null (^−/−) mutant mice

Gatzinsky

Holtmann

Daraie

et al. 2003

Glia

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The nodes of Ranvier are sites of specific interaction between Schwann cells and axons. Besides their crucial role in transmission of action potentials, the nodes of Ranvier and in particular the paranodal axon-Schwann cell networks (ASNs) are thought to function as local centers in large motor axons for removal, degradation, and disposal of organelles. In order to test whether ciliary neurotrophic factor (CNTF), which is present at high levels in the Schwann cell cytoplasm, is involved in the maintenance of these structures, we have examined lumbar ventral root nerve fibers of alpha-motor neurons by electron microscopy in 3- and 9-month-old Cntf null ((-/-)) mutant mice. Nerve fibers and nodes of Ranvier in 3-month-old Cntf(-/-) mutants appeared morphologically normal, except that ASNs were more voluminous in the mutants than in wild-type control animals at this age. In 9-month-old Cntf(-/-) animals, morphological changes, such as reduction in nerve fiber and axon diameter, myelin sheath disruption, and loss of ASNs at nodes of Ranvier, were observed. These findings suggest that endogenous CNTF, in addition to its role in promoting motor neuron survival and regeneration, is needed for long-term maintenance of alpha-motor nerve fibers. The premature loss of paranodal ASNs in animals lacking CNTF, which seems to be a defect related to a disturbed interaction in the nodal region between the axon and its myelinating Schwann cells, could impede the maintenance of a normal milieu in the motor axon, preceding more general neuronal damage.

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“…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%

Removal of retrogradely transported material from rat lumbosacral alpha-motor axons by paranodal axon-schwann cell networks

1997

Glia

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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

Cited by 70 publications

References 30 publications

Functional consequences of repeated organophosphate exposure: Potential non-cholinergic mechanisms

Functional consequences of repeated organophosphate exposure: Potential non-cholinergic mechanisms

Early onset of degenerative changes at nodes of Ranvier in alpha‐motor axons of Cntf null (^−/−) mutant mice

Removal of retrogradely transported material from rat lumbosacral alpha-motor axons by paranodal axon-schwann cell networks

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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

Cited by 70 publications

References 30 publications

Functional consequences of repeated organophosphate exposure: Potential non-cholinergic mechanisms

Functional consequences of repeated organophosphate exposure: Potential non-cholinergic mechanisms

Early onset of degenerative changes at nodes of Ranvier in alpha‐motor axons of Cntf null (−/−) mutant mice

Removal of retrogradely transported material from rat lumbosacral alpha-motor axons by paranodal axon-schwann cell networks

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Early onset of degenerative changes at nodes of Ranvier in alpha‐motor axons of Cntf null (^−/−) mutant mice