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Journal of Neuroscience, Vol 14, 3672-3687, Copyright © 1994 by Society for Neuroscience
Injury-induced plasticity of spinal reflex activity: NK1 neurokinin receptor activation and enhanced A- and C-fiber mediated responses in the rat spinal cord in vitro
SW Thompson, A Dray and L Urban
Sandoz Institute for Medical Research, London, United Kingdom.
A- and C-fiber evoked ventral root potential (VRP) responses have been
examined in isolated spinal cord preparations maintained in vitro that were
taken from young rats in which behavioral hyperalgesia (thermal and
mechanical) was induced following UV irradiation of one hindpaw. Evoked
VRPs were compared with those in naive untreated animals. The duration of
both the A- and C-fiber evoked VRP was significantly increased in
UV-treated animals. The amplitude of the summated VRP evoked by repeated
low-frequency (1.0-5.0 Hz) C-fiber stimulation, a measure of windup, was
significantly greater in UV-treated animals. In UV-treated animals,
repeated low-frequency (1.0-5.0 Hz) stimulation of A-fiber inputs to the
spinal cord also evoked a significant summated VRP, which was not observed
in spinal cords from untreated animals. In naive animals the prolonged VRP
evoked following single shock C-fiber stimulation was significantly
antagonized by the NMDA receptor antagonist D-AP5 and the NK2 receptor
antagonist MEN, 10376 but not by the NK1 receptor antagonists CP-96,345 or
RP,67580. Summated VRPs evoked by repeated C-fiber stimulation in naive
animals were significantly antagonized only by D-AP5. In hyperalgesic
animals the prolonged VRP evoked by C-fiber stimulation was significantly
reduced by NK1, NK2, and NMDA antagonists. The summated VRP was also
significantly reduced by these antagonists. In both untreated and UV-
irradiated animals the single shock evoked A-fiber ventral root response
was significantly antagonized only by D-AP5. However, the summated VRP
evoked by repeated A-fiber stimulation in UV-treated animals was also
significantly reduced by NMDA, NK1, and NK2 receptor antagonists. The
present study has demonstrated enhanced A- and C-fiber evoked responses in
the rat spinal cord in vitro following induction of a peripheral injury by
UV irradiation and which was associated with behavioral hyperalgesia to
thermal and mechanical stimuli. Under this condition, repetitive
stimulation of A-fiber primary afferents was capable of producing an
enhancement of spinal excitability similar to that evoked by C-fibers in
normal animals. Furthermore, we have observed the expression of an NK1
receptor component to the C-fiber evoked response following the
establishment of the peripheral injury. The enhanced ventral root responses
and changes in receptor sensitivity may contribute to the phenomenon of
central sensitization and may be directly related to the behavioral
hyperalgesia observed. Moreover, these findings may be relevant to the
mechanisms of enhanced central excitability that occur in clinical
conditions of inflammatory hyperalgesia and neuropathic pain.
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