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Volume 16, Number 16,
Issue of August 15, 1996
pp. 5189-5195
Copyright ©1996 Society for Neuroscience
Collateral Sprouting of Uninjured Primary Afferent A-Fibers into
the Superficial Dorsal Horn of the Adult Rat Spinal Cord after Topical
Capsaicin Treatment to the Sciatic Nerve
Received April 4, 1996; revised May 30, 1996; accepted June 3, 1996.
Richard J. Mannion1,
Tim P. Doubell1,
Richard E. Coggeshall2, and
Clifford J. Woolf1
1 Department of Anatomy and Developmental Biology,
University College London, London WC1E 6BT, United Kingdom, and
2 Department of Anatomy and Neurosciences, Marine
Biomedical Institute, The University of Texas Medical Branch,
Galveston, Texas 77555-1069
That terminals of uninjured primary sensory neurons terminating in
the dorsal horn of the spinal cord can collaterally sprout was first
suggested by , but this has since been disputed.
Recently, horseradish peroxidase conjugated to the B subunit of cholera
toxin (B-HRP) and intracellular HRP injections have shown that sciatic
nerve section or crush produces a long-lasting rearrangement in the
organization of primary afferent central terminals, with A-fibers
sprouting into lamina II, a region that normally receives only C-fiber
input (). The mechanism of this A-fiber sprouting has
been thought to involve injury-induced C-fiber transganglionic
degeneration combined with myelinated A-fibers being conditioned into a
regenerative growth state.
In this study, we ask whether C-fiber degeneration and A-fiber
conditioning are both necessary for the sprouting of A-fibers into
lamina II. Local application of the C-fiber-specific neurotoxin
capsaicin to the sciatic nerve has previously been shown to result in
C-fiber damage and degenerative atrophy in lamina II. We have used
B-HRP to transganglionically label A-fiber central terminals and have
shown that 2 weeks after topical capsaicin treatment to the sciatic
nerve, the pattern of B-HRP staining in the dorsal horn is
indistinguishable from that seen after axotomy, with lamina II
displaying novel staining in the identical region containing
capsaicin-treated C-fiber central terminals.
These results suggest that after C-fiber injury, uninjured
A-fiber central terminals can collaterally sprout into lamina II of the
dorsal horn. This phenomenon may help to explain the pain associated
with C-fiber neuropathy.
Key words:
regeneration;
pain;
plasticity;
sensory neuron;
injury;
C-fiber
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