Slow Axonal Transport of Neurofilament Proteins: Impairment of β,β′-Iminodipropionitrile Administration

Griffin, John W.; Hoffman, Paul N.; Clark, Arthur W.; Carroll, P.; Price, Donald L.

doi:10.1126/science.81524

Cited by 340 publications

(143 citation statements)

References 16 publications

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“…The transport profiles were followed to 135 d after labeling and were interpreted as showing only progressive anterograde movement of the labeled proteins. Subsequent reports of slow axonal transport showed similar profiles demonstrating proximal to distal movement of cytoskeletal proteins (Ochs and Johnson, 1969;Griffin et al, 1978Griffin et al, , 1982Griffin et al, , 1984Lasek et al, 1992). These pulse-labeling experiments did not, however, preclude the existence of a retrograde slow component.…”

Section: Discussionmentioning

confidence: 64%

Retrograde transport of radiolabeled cytoskeletal proteins in transected nerves

Glass

Griffin

1994

J. Neurosci.

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Slow axonal transport is the mechanism by which cytoskeletal proteins are distributed within the axon. This function has traditionally been considered an exclusively unidirectional, anterograde process. Previous observations of cytoskeletal redistribution in surviving, transected axons of the C57BL/Ola mouse led us to hypothesize a retrograde component of cytoskeletal transport. To test this hypothesis against previous methods of measuring slow transport of cytoskeleton, we radioactively pulse-labeled proteins in sensory neurons of C57BL/Ola mice and followed their redistribution by gel fluorography in ligated and unligated sciatic nerves. Slow axonal transport of cytoskeletal proteins proceeded with the same characteristics in C57BL/Ola as in standard C57BL/6 mice. In comparison to the transport profiles from unligated control nerves, in ligated nerves there was redistribution of radiolabeled neurofilament and tubulin proteins back toward the cell body during the 14 d experimental period. These observations demonstrate that pulse-labeled cytoskeletal proteins move bidirectionally in this experimental system, and may provide insight into the normal mechanisms of cytoskeletal maintenance.

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Section: Discussionmentioning

confidence: 64%

Retrograde transport of radiolabeled cytoskeletal proteins in transected nerves

Glass

Griffin

1994

J. Neurosci.

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“…The neurofilaments become located almost exclusively at the perimeter of the axon and the microtubules are located at the center of the axon (49). At appropriate doses, IDPN selectively blocks movement ofthe neurofilaments but has very little effect on the transport of tubulin and SCb proteins (26). The neurofilaments accumulate in large masses at the proximal end of the axon near the cell body (27).…”

Section: ##'-Iminodiproprionitrile Interferes With the Coordinate Momentioning

confidence: 99%

“…For example, the neurotoxin #,#'-iminodiproprionitrile (IDPN) causes the neurofilaments and microtubules to segregate (26,27,49). The neurofilaments become located almost exclusively at the perimeter of the axon and the microtubules are located at the center of the axon (49).…”

Section: ##'-Iminodiproprionitrile Interferes With the Coordinate Momentioning

confidence: 99%

Axonal transport of the cytoplasmic matrix.

Lasek¹,

Garner²,

Brady³

1984

The Journal of Cell Biology

283

155

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The cytoplasmic matrix is often highly specialized, making it possible to clearly relate particularaspects ofthe cytoplasmic matrix to the specialized functions of cells . For example, in striated muscle cells the contractile components of the cytoplasmic matrix dominate the cell structurally and functionally. Neurons are another example of cells in which specializations of structure and function can be clearly related to particular aspects of the cytoplasmic matrix (36, 37). The primary function of neurons is to convey information from one location in the organism to another. Pathways for information transfer in the nervous system are provided by specialized neuronal extensions, the axons and the dendrites . Axons, in particular, are specialized to convey information over very long distances, meters in some cases. Accordingly, in the axon the cytoplasmic matrix is specialized to generate and support the extremely elongate shape ofthe axon during development, regeneration, and maturity.To generate and maintain the great volume of cytoplasm within the axon, neurons must produce tremendous amounts of protein (32). Essentially all axonal proteins are synthesized in the neuron cell body and then conveyed into the axon by axonal transport, which provides a lifeline for the axon and its terminus (25,36). Axonal transport is a process that is initiated when the axon first develops and that continues throughout the life of the neuron. To meet the needs of large animals, which require long axons, axonal transport has become one of the most highly developed mechanisms for the intracellular transport of materials in metazoan cells .

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“…The neuronal necrosis, phagocytosis and loss observed in our material indicate that irreversible changes often occur. Proximal axonal swellings filled with neurofilaments may reflect an impaired axonal transport of cytoskeletal proteins (12). such impairment might be related to a deficient energy supply, due to decreased activity of the copper containing enzyme cytochrome oxidase, as has been demonstrated in motor neurons in swayback in sheep (11) and goats (16).…”

mentioning

confidence: 99%

Delayed swayback in goat kids, a study of 23 cases

Wouda

Borst²,

Gruys

1986

Veterinary Quarterly

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SUMMARY The results of a retrospective study of 23 goat kids with delayed swayback are reported. Principal clinical signs were ataxia, loss of postural control, spasticity of the hindlimbs, and muscular weakness, often progressing to permanent recumbency. Denervation of skeletal muscles was demonstrated by electromyography in 2 kids. Three kids slowly recovered during hospitalisation. Histopathological changes were characterized by degeneration of selected neuronal populations with their processes within the central and the peripheral nervous system. Affected systems included upper motor neuron, vestibular, general proprioceptive, and lower motor neuron pathways, with additional involvement of the cerebellar cortex in some animals. Our findings, including limited ultrastructural observations, support the notion that the neuraxon rather than the myelin sheath is the prime target of disease in delayed swayback. The available copper values of affected kids and their unaffected herd mates were significantly lower than those of random control goats, which provides furt her support for a role of copper deficiency in the aetiology of this disease in the goat.

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Slow Axonal Transport of Neurofilament Proteins: Impairment of β,β′-Iminodipropionitrile Administration

Cited by 340 publications

References 16 publications

Retrograde transport of radiolabeled cytoskeletal proteins in transected nerves

Retrograde transport of radiolabeled cytoskeletal proteins in transected nerves

Axonal transport of the cytoplasmic matrix.

Delayed swayback in goat kids, a study of 23 cases

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