This study investigates the antinociception caused by intradermal (i.d) or intracerebroventricular (i.c.v.) injection of the capsaicin receptor antagonist capsazepine (CPZ), and ruthenium red (RR) (a cation-selective antagonist coupled to vanilloid receptor of capsaicin), on the chemical nociception caused by i.d. injection of formalin (FM) and capsaicin (CAP) into the mouse paw. The i.d. injection of either CPZ or RR in association with FM or CAP, inhibited the early phase, and to a lesser extent the late phase, of the FM, as well as CAP-induced nociception. Given i.c.v., both CPZ and RR caused discrete antinociception in the FM (both phases), while producing graded inhibition of CAP. The actions of CPZ and RR were insensitive to i.p. injection of naloxone (5 mg/kg). These results indicate that i.d. injection of CPZ and RR produce marked antinociception in chemical models of neurogenic pain induced by CAP and FM in mice. However, administered by supraspinal site, both CPZ and RR were inactive in inhibiting FM, but prevented, in a graded manner, CAP-induced algesic response, suggesting the participation of distinct mechanisms in the nociception induced by FM and CAP. Thus, vanilloid selective antagonists seem to be useful tools for investigating the nociception elicited by CAP and FM.