The site of action of morphine and indomethacin differs with electrical stimulation of cutaneous or tibial nerves in normal and adjuvant arthritic rats.

Evoked potentials were recorded from the ventrobasal (VB) thalamus in normal and adjuvant arthritic rats anaesthetized with urethane (1200 mg/kg, i.p.). Effects of morphine and indomethacin on the evoked potentials elicited by transcutaneous electrical stimulation (TES) or tibial nerve electrical stimulation (TNES) were investigated. Morphine (1-3 mg/kg, i.v.) significantly depressed the potentials evoked by TES an TNES, in both groups. The magnitudes of the depressant effect of morphine were roughly equivalent, in each experiment. In normal rats, indomethacin (3-10 mg/kg, i.v.) significantly depressed the evoked potentials elicited by TES, but did not depress the evoked potentials elicited by TNES. In adjuvant arthritic rats, indomethacin (1-10 mg/kg, i.v.) depressed the evoked potentials elicited by TES and also, be it less readily, those elicited by TNES effects were more readily produced by TES than by TNES. These results suggest that the site of action of indomethacin differs in normal and adjuvant arthritic rats. The central antinociceptive action of indomethacin is clearly detectable in the presence of chronic inflammation. The antinociceptive action of morphine may reside in the neo-spinothalamic projection system, in both groups of rats.