The Journal of Neuroscience, September 15, 1998, 18(18):7581-7587
Inflammatory Mediators Sensitize Acutely Axotomized Nerve Fibers
to Mechanical Stimulation in the Rat
Martin
Michaelis,
Carola
Vogel,
Karl-Heinz
Blenk,
Adalsteinn
Arnarson, and
Wilfrid
Jänig
Physiologisches Institut, Christian-Albrechts-Universität,
24098 Kiel, Germany
Many axotomized myelinated as well as unmyelinated cutaneous nerve
fibers are sensitive to mechanical stimuli applied to the cut nerve end
within a few hours after nerve lesion. Here we investigated the
influence of inflammatory mediators on this ectopic mechanosensitivity after cutting and ligating the sural nerve in anesthetized rats. Neural
activity was recorded from single axons in filaments teased from the
sural or sciatic nerve proximally to the lesion site 2-33 hr after
axotomy. Using calibrated von Frey hairs (1.0-128.5 mN), 30 sec trains
of phasic stimuli were applied to the cut nerve end immediately before
and after local application of a mixture of inflammatory mediators
[inflammatory soup (IS), consisting of bradykinin, 5-HT, prostaglandin
E2, histamine (all 10 µM), and
K+ 7 mM, pH 7.0] for 2 min. Before as
well as after IS application, von Frey thresholds were significantly
lower in myelinated (A) fibers than in unmyelinated (C) fibers. IS
application enhanced the ectopic mechanical excitability, as expressed
in reduced von Frey thresholds and increased response magnitudes, of
most severed mechanosensitive C fibers (77%) and some mechanosensitive
A fibers (46%). The sensitization lasted for 10-40 min after a 2 min
IS application. Additionally, among axotomized nerve fibers
unresponsive to probing of the nerve lesion site before IS application,
1 of 63 (1.6%) A and 3 of 106 (2.8%) C fibers became mechanosensitive immediately after IS application. The results indicate that after axotomy, inflammatory processes augment touch-evoked ectopic activity in lesioned sensory nerve fibers. Because many affected afferents are
presumably of nociceptive function, their enhanced neural barrage may
contribute to neuropathic pain states.
Key words:
axotomy; hyperalgesia; inflammation; sensitization; pain; electrophysiology
Copyright © 1998 Society for Neuroscience 0270-6474/98/18187581-07$05.00/0
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