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

The effect of gliquidone, an ATP-dependent K+ (K(ATP)) channel blocker , on morphine-induced hypermotility in mice was studied. Morphine (5-4 0 mg/kg s.c.) dose dependently increased ambulatory activity. Gliquido ne (10 mug/mouse i.c.v.) induced a parallel displacement to the right of the morphine dose-response curve. Moreover, gliquidone (10 and 40 m ug/mouse i.c.v.) produced a dose-dependent antagonism of morphine (20 mg/kg s.c.)-induced hypermotility. These results suggest that K(ATP) c hannels are involved in morphine-induced hypermotility. The present da ta, together with those of previous studies showing antagonism by K(AT P) channel blockers of morphine-induced antinociception and hypertherm ia, further indicate that the opening of K(ATP) channels plays an impo rtant role in the mechanism of action of morphine.