Nociceptin is the endogenous
ligand of a new
opioid receptor, the
opioid receptor-like-1 (
ORL1) receptor. Chronic inflammatory
pain causes an increase in the expression of
nociceptin and the
ORL1 receptor in the dorsal horn of rat spinal cord, thus indicating an involvement of the endogenous
nociceptin/ORL1 system in mechanisms of pathological
pain. This study investigates the influence of
neuropathic pain on the expression of
nociceptin using immunohistochemistry. To induce
neuropathic pain, a
ligation of the sciatic nerve was performed in 12 rats under
general anesthesia. A
sham operation was performed in 12 rats of the control group. Nerve
ligation caused a significant ipsilateral
thermal hyperalgesia, a typical sign of
neuropathic pain. The paw withdrawal latency was decreased by 45.7+/-4.9% ( p<0.05) at day 5 and by 37.3+/-1.8% ( p<0.05) at day 10. Although
hyperalgesia was fully present after 5 days, no changes in
nociceptin immunoreactivity in the lumbar spinal cord were detected at this time point. Ten days after nerve
ligation, there was a 2.46+/-0.38 fold ( p<0.05) bilateral increase in
nociceptin immunoreactivity in the lamina superficiales (I and II), with a notable increase in the inner lamina II at the level of L4. Further investigations are necessary to elucidate the relationship between
neuropathic pain, the nociceptin-ORL1 receptor system and potential therapeutic options.