BACKGROUND: Plantar hindpaw incision produces hyperalgesia, transient upregulation of cyclooxygenase-2 (COX-2) and prolonged upregulation of cyclooxygenase-1 (COX-1) in rat lumbar spinal cord. Our hypothesis in this study was that a deep thoracic incision causes COX-1 and COX-2 upregulation in the dorsal horn coincident with pain-related behavior, and that specific cell types contribute to this increase in COX expression. METHODS: A left lateral thoracic skin incision was made in anesthetized rats, and superficial and deep muscles were incised. Postoperative pain-related behavior was quantified by recording exploratory rearing. Four and 24 h postsurgery, COX-1 and COX-2 immunohistochemistry, with co-labeling for cell type, were performed on the spinal cord. RESULTS: Deep thoracic muscle incision produced a 42% decrease in rearing compared to sham skin-incision controls at 4 h postsurgery (P = 0.001). There was an increase in both COX-1 and COX-2 immunoreactivity in the thoracic dorsal horn at 4 h postsurgery on the ipsilateral side of surgery animals compared to the ipsilateral side of control animals, contralateral side of surgery animals or contralateral side of control animals. No surgery-induced differences were seen at the lumbar level. At 24 h postsurgery, there was no longer a decrease in rearing, and no surgery-induced differences in COX-1 or COX-2 were seen at any level. At 4 h postsurgery, 96% of COX-1 immunoreactive cells co-localized with microglia and 98% of COX-2 immunoreactive cells co-localized with neurons. CONCLUSIONS: A unilateral deep thoracic wound produces pain-related behavior and, at the same time, ipsilateral upregulation of microglial COX-1 and neuronal COX-2 in the thoracic dorsal horn.
BACKGROUND: Plantar hindpaw incision produces hyperalgesia, transient upregulation of cyclooxygenase-2 (COX-2) and prolonged upregulation of cyclooxygenase-1 (COX-1) in rat lumbar spinal cord. Our hypothesis in this study was that a deep thoracic incision causes COX-1 and COX-2 upregulation in the dorsal horn coincident with pain-related behavior, and that specific cell types contribute to this increase in COX expression. METHODS: A left lateral thoracic skin incision was made in anesthetized rats, and superficial and deep muscles were incised. Postoperative pain-related behavior was quantified by recording exploratory rearing. Four and 24 h postsurgery, COX-1 and COX-2 immunohistochemistry, with co-labeling for cell type, were performed on the spinal cord. RESULTS: Deep thoracic muscle incision produced a 42% decrease in rearing compared to sham skin-incision controls at 4 h postsurgery (P = 0.001). There was an increase in both COX-1 and COX-2 immunoreactivity in the thoracic dorsal horn at 4 h postsurgery on the ipsilateral side of surgery animals compared to the ipsilateral side of control animals, contralateral side of surgery animals or contralateral side of control animals. No surgery-induced differences were seen at the lumbar level. At 24 h postsurgery, there was no longer a decrease in rearing, and no surgery-induced differences in COX-1 or COX-2 were seen at any level. At 4 h postsurgery, 96% of COX-1 immunoreactive cells co-localized with microglia and 98% of COX-2 immunoreactive cells co-localized with neurons. CONCLUSIONS: A unilateral deep thoracic wound produces pain-related behavior and, at the same time, ipsilateral upregulation of microglial COX-1 and neuronal COX-2 in the thoracic dorsal horn.