In this electrophysiological study, the effect of BU-224 (2-(4,5-dihydroimidazol-2yl)-quinoline hydrochloride)), a novel high affinity imidazoline I2 receptor ligand, was tested on the responses of nociceptive neurones in the spinal dorsal horn. When applied spinally, akin to an intrathecal application (i.t.), BU-224 (5-250 microg) reduced the nociceptive responses of dorsal horn neurones, producing a dose-dependent inhibition of C-fibre evoked responses, postdischarge and wind-up of the cells. A complete block of the antinociceptive effects was produced when idazoxan (100 microg), with both alpha2-adrenoceptor and imidazoline I2 receptor antagonist actions, was administered i.t. 10 min prior to the maximal dose of BU-224 tested. The nonselective alpha2-adrenoceptor antagonist, yohimbine (150 microg) only partially attenuated the inhibitory effects of BU-224 when administered i.t. 10 min prior. The highly selective alpha2-adrenoceptor antagonist, atipamezole (100 microg) produced no greater reversal than yohimbine under the same conditions. Although BU-224 has been reported to possess high affinity for imidazoline I2 receptors, a minor action at spinal alpha2-adrenoceptor receptors cannot be discounted. These results demonstrate that BU-224 is an agonist and that imidazoline I2 receptors, present in the dorsal horn, might play a role in spinal nociception, although further studies are needed to fully elucidate their functional roles.