For 15 units, Diffuse Noxious Inhibitory Controls (DNIC)^67,68 were investigated by applying noxious thermal stimuli (52 °C) to the distal two-thirds of the tail. This conditioning stimulus induced strong inhibition of the responses to both Aα (28%) and C (71%) fibres. Post-effects of long duration were commonly observed after cessation of the conditioning stimulus. The systemic injection of naloxone (0.3 mg/kg, i.v.) resulted in a partial reduction in these inhibitory effects with a decrease of about 50% for both Aα and C fibre response 10 min after naloxone administration. This was followed by a progressive recovery lasting 30 min.

28 convergent units, including the 15 reported above, were recorded to investigate t the effect of naloxone upon the unconditioned response. Responses to Aα fibre were unaffected, whereas the responses to C fibre were slightly (17%) but significantly increased by naloxone.

These results suggest that the transmission of nociceptive messages at the spinal level is modulated by and/or dependent upon endogenous opiates. In the light of our previous suggestion⁶⁸ that the contrast between the activities of two pools of units might be the pain signalling output from the convergent dorsal horn neurones, it is suggested that pain transmission is dependent on at least two complementary systems, both involving endogenous opiates. The opposite functional actions of these two systems might explain the bidirectional effects of naloxone upon nociception reported in the literature.