1 The eects of intravenous sufentanil and pre-administration of N-methyl-D-aspartate (NMDA) receptor antagonists were tested on a re¯ex triggered by C-®bre activation. The re¯ex was elicited by electrical stimulation of the sural nerve and recorded from the ipsilateral biceps femoris muscle in halothane anaesthetized rats either (1) with an intact neuraxis or (2) in which the brain had previously been transected at the level of the obex. 2 All four doses of sufentanil (0.33, 0.6, 1 and 2 mg kg
71) elicited a depression of the re¯ex in a dose-dependent manner. However, following the expected depression, all doses of sufentanil elicited both facilitation of the re¯ex and tonic inter-stimulus discharges. 3 The C-®bre re¯ex was not modi®ed following intravenous ketamine (1 mg kg
71) or (+)-HA966 (5 or 10 mg kg
71) but, when administered 5 min before sufentanil, these drugs enhanced both the extent and the duration of the depression and strongly reduced the facilitations. 4 In the obex-transected rats, the depressive eect of 1 mg kg 71 sufentanil increased, while the facilitation of the C-®bre re¯ex and the tonic inter-stimulus discharges disappeared. Preadministration of 10 mg kg 71 (+)-HA966 reinforced and prolonged the depressive eect of sufentanil. 5 These results extend previous studies suggesting the involvement of NMDA receptors in the spinal transmission of nociceptive signals. They illustrate the potential of spinal NMDA receptor blockade to both enhance the analgesic, and prevent the pro-nociceptive, eects of sufentanil.