A C-fiber reflex elicited by electrical stimulation within the territory of the ipsilateral sural nerve, was recorded from the biceps femoris muscle in anesthetized rats. The temporal evolution of the reflex was studied using a constant level of stimulus intensity (3 x threshold) and recruitment curves were built by varying stimulus intensity from 0 to 7 x threshold. Intrathecal doses of buprenorphine in the 0.2 to 10 micrograms range, elicited a facilitation of the C-fiber reflex in a dose-dependent manner. A large dose (100 micrograms) depressed but did not block the reflex. Intracerebroventricular doses of buprenorphine in the 0.1 to 10 micrograms range, facilitated the C-fiber reflex. A higher dose (100 micrograms) elicited a biphasic effect: depressive when the stimulus intensity was weak and facilitatory when the stimulus intensity was strong. It is concluded that the antinociceptive properties of buprenorphine cannot be related to a direct or indirect depressive spinal effect. In terms of spinal and supraspinal effects of buprenorphine, it is likely that buprenorphine facilitates the C-fiber reflex via a supraspinal mechanism that acts on sensory and/or motor components of the reflex arc although the depression of the reflex involves a spinal mechanism. The lipophilic properties of buprenorphine could explain a substantial diffusion from its spinal injection site to the brain. From a clinical standpoint, this study confirms that intrathecal administration of buprenorphine is an inadequate way of accessing spinal opioid receptors.