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Neural architecture in transected rabbit sciatic nerve after prolonged nonreinnervation

Published online by Cambridge University Press:  01 May 1998

J. L. BRADLEY
Affiliation:
Clinical Neurosciences, Royal Free Hospital School of Medicine, London, UK
D. A. ABERNETHY
Affiliation:
Clinical Neurosciences, Royal Free Hospital School of Medicine, London, UK
R. H. M. KING
Affiliation:
Clinical Neurosciences, Royal Free Hospital School of Medicine, London, UK
J. R. MUDDLE
Affiliation:
Clinical Neurosciences, Royal Free Hospital School of Medicine, London, UK
P. K. THOMAS
Affiliation:
Clinical Neurosciences, Royal Free Hospital School of Medicine, London, UK
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Abstract

Observations have been made on the rabbit sciatic nerve distal to a transection, with survival periods of up to 26 mo and prevention of reinnervation. It was confirmed that the nerve becomes compartmented by fibroblast processes and that a zone of fine collagen fibrils develops around the Schwann cell columns that constitute the Büngner bands. The Schwann cells become progressively more atrophic but after 6 mo of denervation still expressed low affinity p75 nerve growth factor receptor (NGFR), the latest stage at which this was examined. NGFR was also expressed by the processes of the fibroblasts producing the endoneurial compartmentation. By 26 mo after transection the site of previous nerve fibres was indicated by sharply demarcated domains of approximately circular outline in transverse section consisting of densely packed longitudinally oriented collagen fibrils. Some of these domains still possessed centrally situated Schwann cells or residual basal lamina but many were acellular. The central collagen fibrils in these domains were of smaller diameter than those situated peripherally but were of larger size than those that form around the Büngner bands during wallerian degeneration. The peripherally located fibrils in the domains were of the same calibre as for normal endoneurial collagen. The collagen domains were encircled by fibroblast processes or at times enclosed in a perineurial cell ensheathment. Long-standing axonal loss therefore leads to a striking reorganisation of the internal architecture of peripheral nerve trunks. The findings may be relevant for the interpretation of the appearances in chronic peripheral neuropathies in man.

Type
Research Article
Copyright
© Anatomical Society of Great Britain and Ireland 1998

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