Somatofugal events in wallerian degeneration: A conceptual overview

Joseph, Barry S.

doi:10.1016/0006-8993(73)90250-3

Cited by 87 publications

(18 citation statements)

References 105 publications

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“…Alternatively, in Wallerian degeneration the Schwann cell is exposed also to axonal debris, lytic enzymes, and potentially a range of molecules that may act as signal factors that specifically initiate a destructive response in Schwann cells (Joseph, 1973;Lubinska and Jastreboff, 1977). In double myelination, completely displaced myelin internodes are maintained long term in normal animals (Heath, 1982;Kidd and Heath, 1988a) and survive degeneration of the axon and inner sheath (Kidd et al,199 1;present results).…”

Section: Discussionmentioning

confidence: 58%

“…In Wallerian degeneration, the mechanisms that initiate the secondary responses of Schwann cells such as myelin breakdown and mitosis have not been established (Bigbee et al, 1987;Oaklander et al, 1987;White et al, 1989;LoPachin et al, 1990) but could involve the loss of axonal contact and of trophic substances normally supplied by the axon (Joseph, 1973;Oaklander and Spencer, 1988). Alternatively, in Wallerian degeneration the Schwann cell is exposed also to axonal debris, lytic enzymes, and potentially a range of molecules that may act as signal factors that specifically initiate a destructive response in Schwann cells (Joseph, 1973;Lubinska and Jastreboff, 1977).…”

Section: Discussionmentioning

confidence: 99%

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Myelin sheath survival following axonal degeneration in doubly myelinated nerve fibers

Kidd

1991

J. Neurosci.

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Axonal contact plays a critical role in initiating myelin formation by Schwann cells. However, recent studies of “double myelination” have indicated that myelin maintenance continues in Schwann cells completely displaced from physical contact with the axon. This raises the possibility either that diffusible trophic factors are produced by the axon, or that the axon is not required for myelin maintenance by these displaced Schwann cells. To test these hypotheses, the axons involved in double myelination in the mouse superior cervical ganglion (SCG) were transected surgically by a transganglionic lesion. The inferior pole of the SCG was resected to limit axonal regeneration. This method produced a typical Wallerian pattern of degeneration in the superior pole, without compromising the blood supply or introducing nonspecific trauma. EM analysis at 1 and 5 d postoperatively showed that initially the axon degenerated, followed by breakdown of the inner myelin sheath. In those configurations where the outer Schwann cell was only partly displaced from the axon, the outer myelin sheath degenerated simultaneously. However, in completely displaced internodes the outer sheath survived degeneration of the axon and inner sheath. Outer internodes remained intact for at least 5 weeks after transection (the longest time point in this study), at which time they enclosed reorganized processes of the inner Schwann cells, their basal lamina, and numerous collagen fibrils. Axonal regeneration within surviving outer internodes was rare and was characterized by the development of typical Remak ensheathment by the inner Schwann cells. We conclude that in the mouse SCG, myelin maintenance does not depend on the continued presence of the axon. These data suggest further that myelin breakdown in Wallerian degeneration may be initiated by mechanisms other than absence of a viable axon.

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Section: Discussionmentioning

confidence: 58%

Section: Discussionmentioning

confidence: 99%

Myelin sheath survival following axonal degeneration in doubly myelinated nerve fibers

Kidd

1991

J. Neurosci.

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“…The main comparative parameter is the velocity of the process. While in PNS WD occurs in hours or days, in CNS it proceeds at a slow rate, lasting for weeks and sometimes months (Donat and Wisniewski 1973, Joseph 1973, Lubinska 1977, David et al 1990, Hall 1993, Reier 1995. Many factors are probably associated with this difference.…”

Section: Discussionmentioning

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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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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“…Originally WD was considered to be a passive process induced by the lack of nutrients and cell-body derived factors following injury(Joseph, 1973). However, discovery of the slow WD mouse (Wld s ) led to the realization that axons degenerate through an active process (Lunn et al, 1989).…”

Section: The Biology Of Wallerian Degenerationmentioning

confidence: 99%

The neuroimmunology of degeneration and regeneration in the peripheral nervous system

et al. 2015

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Peripheral nerves regenerate following injury due to the effective activation of the intrinsic growth capacity of the neurons and the formation of a permissive pathway for outgrowth due to Wallerian degeneration. Wallerian degeneration and subsequent regeneration are significantly influenced by various immune cells and the cytokines they secrete. Although macrophages have long been known to play a vital role in the degenerative process, recent work has pointed to their importance in influencing the regenerative capacity of peripheral neurons. In this review, we focus on the various immune cells, cytokines, and chemokines that make regeneration possible in the peripheral nervous system, with specific attention placed on the role macrophages play in this process.

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Somatofugal events in wallerian degeneration: A conceptual overview

Cited by 87 publications

References 105 publications

Myelin sheath survival following axonal degeneration in doubly myelinated nerve fibers

Myelin sheath survival following axonal degeneration in doubly myelinated nerve fibers

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

The neuroimmunology of degeneration and regeneration in the peripheral nervous system

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