GLIQUIDONE, AN ATP-DEPENDENT K+ CHANNEL ANTAGONIST, ANTAGONIZES MORPHINE-INDUCED HYPERMOTILITY

The effect of gliquidone, an ATP-dependent K+ (K(ATP)) channel blocker, on morphine-induced hypermotility in mice was studied. Morphine (5-40 mg/kg s.c.) dose dependently increased ambulatory activity. Gliquidone (10 mug/mouse i.c.v.) induced a parallel displacement to the right of the morphine dose-response curve. Moreover, gliquidone (10 and 40 mug/mouse i.c.v.) produced a dose-dependent antagonism of morphine (20 mg/kg s.c.)-induced hypermotility. These results suggest that K(ATP) channels are involved in morphine-induced hypermotility. The present data, together with those of previous studies showing antagonism by K(ATP) channel blockers of morphine-induced antinociception and hyperthermia, further indicate that the opening of K(ATP) channels plays an important role in the mechanism of action of morphine.