Persistence of Neuromuscular Junctions after Axotomy in Mice with Slow Wallerian Degeneration (C57BL/Wlds)

R. R. Ribchester, Jack Tsao, J. A. Barry, N. Asgari‐Jirhandeh, V. H. Perry, M. C. Brown

Research output: Contribution to journalArticle

46 Citations (Scopus)

Abstract

The present study was undertaken to examine the fate of neuromuscular junctions in C57BL/Wlds mice (formerly known as OLA mice) after nerve injury. When a peripheral nerve is injured, the distal axons normally degenerate within 1‐3 days. For motor axons, an early event is deterioration of motor nerve terminals at neuromuscular junctions. Previously, the vulnerability of motor terminals has been attributed either to a ‘signal’originating at the site of nerve injury and transported rapidly to the terminals or to their continual requirement for essential maintenance factors synthesized in the motor neuron cell body and supplied to the terminals by fast axonal transport. Mice of the Wlds strain have normal axoplasmic transport but show an abnormally slow rate of axon and myelin degeneration. Structure and function are retained in the axons of distal nerve stumps for several days or even weeks after nerve injury in these mice. The results of the present study show that Wlds neuromuscular junctions are also preserved and continue to release neurotransmitter and recycle synaptic vesicle membrane for at least 3 days and in some cases up to 2 weeks after nerve injury. Varying the site of the nerve lesion delayed degeneration by ‐1‐2 days per centimetre of distal nerve remaining. These findings suggest that the mechanisms of nerve terminal degeneration after injury are more complex than can be accounted for simply by the failure of motor neuron cell bodies to supply their terminals with essential maintenance factors. Rather, the data support the view that nerve section normally activates cellular components or processes already present, but latent, in motor nerve endings, and that in Wlds mice either the trigger or the cellular response is abnormal.

Original languageEnglish (US)
Pages (from-to)1641-1650
Number of pages10
JournalEuropean Journal of Neuroscience
Volume7
Issue number7
DOIs
StatePublished - Jan 1 1995

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Wallerian Degeneration
Axotomy
Neuromuscular Junction
Axons
Wounds and Injuries
Axonal Transport
Motor Neurons
Maintenance
Synaptic Membranes
Nerve Degeneration
Nerve Endings
Synaptic Vesicles
Myelin Sheath
Inbred C57BL Mouse
Peripheral Nerves
Neurotransmitter Agents

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)

Cite this

Persistence of Neuromuscular Junctions after Axotomy in Mice with Slow Wallerian Degeneration (C57BL/Wlds). / Ribchester, R. R.; Tsao, Jack; Barry, J. A.; Asgari‐Jirhandeh, N.; Perry, V. H.; Brown, M. C.

In: European Journal of Neuroscience, Vol. 7, No. 7, 01.01.1995, p. 1641-1650.

Research output: Contribution to journalArticle

Ribchester, R. R. ; Tsao, Jack ; Barry, J. A. ; Asgari‐Jirhandeh, N. ; Perry, V. H. ; Brown, M. C. / Persistence of Neuromuscular Junctions after Axotomy in Mice with Slow Wallerian Degeneration (C57BL/Wlds). In: European Journal of Neuroscience. 1995 ; Vol. 7, No. 7. pp. 1641-1650.
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