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Consequences of slow wallerian degeneration for regenerating motor and sensory axons

Consequences of slow wallerian degeneration for regenerating motor and sensory axons
Consequences of slow wallerian degeneration for regenerating motor and sensory axons

The time course of Wallerian degeneration in the tibial and saphenous nerves was compared in Balb/c mice and mice of the C57BL/Ola strain (Lunn et al., 1989). Axons, particularly myelinated ones, in nerves of C57BL/Ola mice are very slow to degenerate, many still being present 3 weeks after axotomy. Nuclear numbers in the distal stump peak much later and do not reach the levels found in Balb/c mice; debris removal is very slow, and Schwann cell numbers only rise slightly above normal levels in the long term. Regeneration was investigated electrophysiologically and by electron microscopy (EM). Myelinated sensory axons regenerated slowly and incompletely compared with motor ones which were only slightly slowed after nerve crush (although they were significantly hindered after nerve section). Total myelinated axon numbers were still some 20% less than normal even after 200 days in sensory nerves. Even after all axons had degenerated in C57BL/Ola mice, regeneration rates of neither myelinated nor unmyelinated sensory axons reached those achieved in Balb/c mice. It is concluded that while regeneration can eventually proceed slowly when Wallerian degeneration is much delayed, the usual rapid time course of Wallerian degeneration is necessary if axons, particularly sensory ones, are to regenerate at optimal rates and to maximum extent. Whilelocal obstruction to axon growth probably impedes the early phase ofregeneration in C57BL/Ola mice, it seems possible that a lack of adequate early signals affects regeneration permanently by minimizing the cell body reaction to injury. © 1992 John Wiley & Sons, Inc.

axon, degeneration, mouse, mutation, regeneration
0022-3034
521-536
Brown, M.C.
98006294-1cd5-4394-ab73-145c06f17f75
Lunn, E.R.
5a327b5f-d724-4d10-9a72-352df4318846
Perry, V.H.
8f29d36a-8e1f-4082-8700-09483bbaeae4
Brown, M.C.
98006294-1cd5-4394-ab73-145c06f17f75
Lunn, E.R.
5a327b5f-d724-4d10-9a72-352df4318846
Perry, V.H.
8f29d36a-8e1f-4082-8700-09483bbaeae4

Brown, M.C., Lunn, E.R. and Perry, V.H. (1992) Consequences of slow wallerian degeneration for regenerating motor and sensory axons. Journal of Neurobiology, 23 (5), 521-536. (doi:10.1002/neu.480230507).

Record type: Article

Abstract

The time course of Wallerian degeneration in the tibial and saphenous nerves was compared in Balb/c mice and mice of the C57BL/Ola strain (Lunn et al., 1989). Axons, particularly myelinated ones, in nerves of C57BL/Ola mice are very slow to degenerate, many still being present 3 weeks after axotomy. Nuclear numbers in the distal stump peak much later and do not reach the levels found in Balb/c mice; debris removal is very slow, and Schwann cell numbers only rise slightly above normal levels in the long term. Regeneration was investigated electrophysiologically and by electron microscopy (EM). Myelinated sensory axons regenerated slowly and incompletely compared with motor ones which were only slightly slowed after nerve crush (although they were significantly hindered after nerve section). Total myelinated axon numbers were still some 20% less than normal even after 200 days in sensory nerves. Even after all axons had degenerated in C57BL/Ola mice, regeneration rates of neither myelinated nor unmyelinated sensory axons reached those achieved in Balb/c mice. It is concluded that while regeneration can eventually proceed slowly when Wallerian degeneration is much delayed, the usual rapid time course of Wallerian degeneration is necessary if axons, particularly sensory ones, are to regenerate at optimal rates and to maximum extent. Whilelocal obstruction to axon growth probably impedes the early phase ofregeneration in C57BL/Ola mice, it seems possible that a lack of adequate early signals affects regeneration permanently by minimizing the cell body reaction to injury. © 1992 John Wiley & Sons, Inc.

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More information

Accepted/In Press date: 20 March 1992
Published date: July 1992
Keywords: axon, degeneration, mouse, mutation, regeneration

Identifiers

Local EPrints ID: 489556
URI: http://eprints.soton.ac.uk/id/eprint/489556
ISSN: 0022-3034
PURE UUID: 07de36a2-bd38-479b-bc33-1422c6830bc1

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Date deposited: 26 Apr 2024 17:04
Last modified: 26 Apr 2024 17:04

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Contributors

Author: M.C. Brown
Author: E.R. Lunn
Author: V.H. Perry

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