Increased spinal
cyclooxygenase activity is associated with nociception induced by tissue
inflammation. In the present study, we examined the changes of
cyclooxygenase-1 and
cyclooxygenase-2 protein expression in several regions of the CNS associated with pain perception, and the role of spinal
cyclooxygenase activity in the development of
allodynia following nerve injury.
Allodynia was induced by
ligation of the left L5 and L6 spinal nerves in rats. Using western blot analysis, we found that the
cyclooxygenase-2 protein levels in the dorsal spinal cord and thalamus (but not in the ventral spinal cord, cingulate cortex and locus coeruleus) increased significantly one day after nerve
ligation, compared with those in the
sham animals. The
cyclooxygenase-2 protein levels in the above tissues were similar in nerve-injured and
sham animals three and 14 days after surgery. In contrast,
cyclooxygenase-1 protein was not detectable in any of the neural tissues examined one, three, and 14 days after nerve injury. In the behavioral experiments, we observed that
intrathecal injection of 100microg of
indomethacin immediately or one day after nerve
ligation attenuated the development of
tactile allodynia. However,
intrathecal injection of
indomethacin had no effect on established
allodynia two weeks after nerve injury.Collectively, our results suggest that
cyclooxygenase-2 is preferentially up-regulated in the dorsal spinal cord and thalamus in response to nerve injury in rats. Spinal
cyclooxygenase-2 probably plays an important role in the early development, but not in the maintenance, of
tactile allodynia caused by the nerve injury in this rat model of
neuropathic pain.