Neuropathic pain induces
allodynia and
hyperalgesia. In the spared nerve injury (SNI) model, marked
mechanical hyperalgesia is manifested as prolongation of the duration of paw withdrawal after pin stimulation. We have previously reported that spinal ventral root discharges (after-discharges) after cessation of noxious mechanical stimulation applied to the corresponding hindpaw were prolonged in anesthetized spinalized rats. Since these after-discharges occurred through transient receptor potential (TRP) V1-positive fibers, these fibers could contribute to
mechanical hyperalgesia. Therefore, we examined whether selective deletion of TRPV1-positive fibers by
resiniferatoxin, an ultrapotent TRPV1 agonist, would affect the behavioral changes and ventral root discharges in SNI rats.
Mechanical allodynia in the von Frey test,
mechanical hyperalgesia after pin stimulation, and enhancement of ventral root discharges, but not
thermal hyperalgesia in the plantar test, appeared in Wistar rats with SNI.
Mechanical hyperalgesia was abolished by treatment with
resiniferatoxin, whereas
mechanical allodynia was not affected. Moreover,
resiniferatoxin eliminated after-discharges completely. These results show that TRPV1-positive fibers do not participate in the
mechanical allodynia caused by sensitization of Aβ-fibers, but contribute to the enhancement of after-discharges and
mechanical hyperalgesia following SNI. It is suggested that the mechanisms responsible for generating
mechanical allodynia differ from those for prolongation of
mechanical hyperalgesia.