M. Ocana et al., GLIQUIDONE, AN ATP-DEPENDENT K-INDUCED HYPERMOTILITY( CHANNEL ANTAGONIST, ANTAGONIZES MORPHINE), European journal of pharmacology, 239(1-3), 1993, pp. 253-255
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.