The effect of diclofenac on the expression of spinal cord c-fos-like immunoreactivity after ischemia-reperfusion-induced acute hyperalgesia in the rat tail

Ischemia-reperfusion of the rat tail for 20 min induces local acute hyperal gesia of approximately 1-h duration. We studied how this stimulus affected the expression of c-fos-like immunoreactivity (c-fos-LI) labeling of neuron s of the sacral spinal cord, and how diclofenac pretreatment influenced the outcome. After ischemia, the number of c-fos-LI-labeled neurons was signif icantly increased when assessed at 60, 90, and 120 min after reperfusion (t o 183%, 283%, and 164% of control, respectively; all P < 0.01). At 90 min, the number of regional c-fos-LI-labeled neurons was increased to 585% in la minae I-II, 183% in laminae III-IV, 270% in laminae V-X, and 286% in total, compared with respective control values (all P < 0.01). After diclofenac p retreatment (subcutaneous 40 mg/Kg, 30 min before insult) the number of c-f os-LI-labeled neurons at 90 min was increased to 424% in laminae I-II, 150% in laminae III-IV, 142% in laminae V-X, and 183% in total tall P ( 0.01). Thus diclofenac pretreatment partially prevented the insult-induced increas e in total and regional neuronal c-fos-LI. This acute nociceptive model inv olves only natural algogens. However, the results were similar to acute che mically induced or chronic adjuvant induced arthritic inflammatory pain mod els in which increases in c-Fos were partially inhibited by nonsteroidal an tiinflammatory drugs.