The Fate of Axonal Debris in Wallerian Degeneration of Rat Optic and Sciatic Nerves

Bignami, A.; Dahl, D.; Nguyen, Bich Tram; Crosby, C. J.

doi:10.1097/00005072-198109000-00005

Cited by 87 publications

(22 citation statements)

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“…the degenerative changes in the cytoskeleton would not present intermediary stages of degeneration. Both dark and watery degeneration as observed in the opossum's crushed optic nerve are similar to what has been observed in many vertebrates (Kruger and Maxwell 1969, Ishise and Rosenbluth 1986, Cook et al 1974, Bignami et al 1981, Cook and Wisniewski 1987, Carrol et al 1992. These studies do not mention the mechanism that would induce one or other type of degeneration, nor do they describe morphological differences between these two patterns of axon degeneration.…”

Section: Discussionsupporting

confidence: 69%

“…In the CNS the cytoskeletal breakdown is thought to promote two morphological aspects of axoplasmic degeneration: (1) "dark degeneration", in which axons become dark, with dense axoplasm, and its content of organelles is very difficult to distinguish, and (2) "watery degeneration", in which axons become pale, enlarged and the axoplasm is either replaced by an amorphous and granular material or is completely devoid of organelles (Kruger and Maxwell 1969, Cook et al 1974, Bignami et al 1981, Malbouisson et al 1984, Cook and Wisniewski 1987, Hasegawa et al 1988). In the PNS however, only "watery degeneration" has been described in the literature (Malbouisson et al 1984(Malbouisson et al , 1985.…”

Section: Introductionmentioning

confidence: 99%

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Watery and dark axons in Wallerian degeneration of the opossum's optic nerve: different patterns of cytoskeletal breakdown?

Narciso

Hokoç

Martínez

2001

An. Acad. Bras. Ciênc.

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In this paper we report a qualitative morphological analysis of Wallerian degeneration in a marsupial. Right optic nerves of opossums Didelphis marsupialis were crushed with a fine forceps and after 24, 48, 72, 96 and 168 hours the animals were anaesthetized and perfused with fixative. The optic nerves were immersed in fixative and processed for routine transmission electron microscopy. Among the early alterations typical of axonal degeneration, we observed nerve fibers with focal degeneration of the axoplasmic cytoskeleton, watery degeneration and dark degeneration, the latter being prevalent at 168 hours after crush. Our results point to a gradual disintegration of the axoplasmic cytoskeleton, opposed to the previous view of an "all-or-nothing" process . We also report that, due to an unknown mechanism, fibers show either a dark or watery pattern of axonal degeneration, as observed in axon profiles. We also observed fibers undergoing early myelin breakdown in the absence of axonal alterations.

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Section: Discussionsupporting

confidence: 69%

Section: Introductionmentioning

confidence: 99%

Watery and dark axons in Wallerian degeneration of the opossum's optic nerve: different patterns of cytoskeletal breakdown?

Narciso

Hokoç

Martínez

2001

An. Acad. Bras. Ciênc.

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“…These membranes are believed to be degraded by proteolysis, which disrupts protein-lipid interactions (23,24). Lipids, including cholesteryl esters, accumulate in many cells of the distal nerve stump, particularly macrophages and Schwann cells, in the form of 0.5-to 2.0-,um lipid droplets, microscopically visible as Marchi-positive granules or sudanophilic, birefringent droplets (25,26). While some of the lipidengorged cells (probably macrophages) leave the site of injury (25,27), many ofthe cells containing the esterified lipid remain in the nerve stump (27,28), where the lipid may be reused during remyelination of regenerating axons (28,29).…”

Section: Discussionmentioning

confidence: 99%

Expression of apolipoprotein E during nerve degeneration and regeneration.

Ignatius¹,

Gebicke‐Härter²,

Skene³

et al. 1986

Proc. Natl. Acad. Sci. U.S.A.

506

252

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A 37-kDa glycoprotein has been described recently, whose synthesis is dramatically increased after injury of the rat sciatic and optic nerves. Cells in the nerve sheath, distal to the site of injury, produce and secrete large amounts of this protein, so that by 3 weeks after injury, it represents 2-5% of the total soluble extracellular protein in the regenerating sciatic nerve sheath, although it fails to accumulate in damaged optic nerve. Results presented here reveal extensive homology between the 37-kDa nerve injury-induced protein and a well-studied serum protein, apolipoprotein E (apoE), that is involved in lipid and cholesterol metabolism and that has been shown recently to be present in adult and developing rat astroglia. Both proteins have identical isoelectric focusing points and similar molecular masses. Antibodies raised against the 37-kDa protein recognize apoE and anti-apoE serum crossreacts with the 37-kDa protein. Sequence data for two 14 amino acid stretches of the 37-kDa protein match identical regions of apoE. These data suggest that the 37-kDa protein is identical to serum apoE and that it could have similar functions to the latter. In the nervous system, for example, it may be involved in the mobilization and reutilization of lipid in the repair, growth, and maintenance of myelin and axonal membranes, both during development and after injury.

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“…This possibility seemed all the more compelling in view of the recent report (Drgtger et al 1983) that neurofilament protein contains an immunologically-recognised ct-MSH-like portion. This protein has been shown to break down in the early stages of the degenerative process (Bignami et al 1981 ;Soifer et al 1981). We therefore investigated the possible presence of an ~-MSHlike principle in the degenerating nerves during the period of 150 kD neurofilament protein breakdown and ct-MSH sensitivity.…”

Section: Introductionmentioning

confidence: 99%

Evidence that the neurotrophic actions of α-MSH may derive from its ability to mimick the actions of a peptide formed in degenerating nerve stumps

Edwards¹,

Zee²,

Verhaagen³

et al. 1984

Journal of the Neurological Sciences

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SUMMARYThe ability of ~-MSH to facilitate the recovery of sensorimotor nerve function following crush lesion is restricted to a critical period following such a lesion. This period coincided with the initiation of sprouting and the disappearance of the 150 kD neurofilament protein from the degenerating distal stump of the nerve.Degenerating nerve contains a factor that is active in a bioassay system for MSH. This factor could not be detected in control nerves.The hypothesis is forwarded that a neurotrophic factor known to be present in degenerating nerve stumps is an ~-MSH-like peptide formed by the breakdown of the 150 kD neurofilament protein.

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The Fate of Axonal Debris in Wallerian Degeneration of Rat Optic and Sciatic Nerves

Cited by 87 publications

References 0 publications

Watery and dark axons in Wallerian degeneration of the opossum's optic nerve: different patterns of cytoskeletal breakdown?

Watery and dark axons in Wallerian degeneration of the opossum's optic nerve: different patterns of cytoskeletal breakdown?

Expression of apolipoprotein E during nerve degeneration and regeneration.

Evidence that the neurotrophic actions of α-MSH may derive from its ability to mimick the actions of a peptide formed in degenerating nerve stumps

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