The profound and prolonged effects of morphine in patients with renal dysfunction have been associated with high plasma levels of the opiate metabolites morphine-6-glucuronide (M6G) and morphine-3-glucuronide (M3G) rather than an increased concentration of morphine. We present here electrophysiological evidence to suggest that potent spinal antinociception can be produced by both M6G and normorphine, another metabolite of morphine. Extracellular recordings of A beta- and C-fibre-evoked responses of convergent dorsal horn neurones were made in the halothane anaesthetised rat. M6G elicited dose-dependent, naloxone-reversible inhibitions of C-fibre-evoked responses which were completely suppressed (8% of control) by 2 micrograms M6G whereas A beta-fibre-evoked responses were only reduced to 57% of controls. The ED50 for the effects of M6G on C-fibre-evoked activity was calculated to be 0.53 micrograms. Systemic administration of M6G (2 mg/kg) also profoundly reduced noxious evoked neuronal activity. Intrathecal normorphine was less potent than M6G but complete selective inhibitions of C-fibre-evoked response could be elicited by 25 micrograms and the ED50 was calculated to be 2.68 micrograms. No such inhibitions were observed following administration of M3G. A comparison with intrathecal morphine in the same preparation reveals that normorphine is equipotent with morphine whereas M6G is 13-fold more potent. These results therefore confirm that M6G and normorphine might be significant contributers to opiate analgesia after administration of morphine.