Gliquidone, an ATP-dependent K+ channel antagonist, antagonizes morphine-induced hypermotility.
The effect of gliquidone, an ATP-dependent K+ (KATP) channel blocker, on morphine-induced hypermotility in mice was studied. Morphine (5-40 mg/kg s.c.) dose dependently increased ambulatory activity. Gliquidone (10 micrograms/mouse i.c.v.) induced a parallel displacement to the right of the morphine dose-response curve. Moreover, gliquidone (10 and 40 micrograms/mouse i.c.v.) produced a dose-dependent antagonism of morphine (20 mg/kg s.c.)-induced hypermotility. These results suggest that KATP channels are involved in morphine-induced hypermotility. The present data, together with those of previous studies showing antagonism by KATP channel blockers of morphine-induced antinociception and hyperthermia, further indicate that the opening of KATP channels plays an important role in the mechanism of action of morphine.
Ocaña
M
M
Department of Pharmacology, Medical School, University of Granada, Spain.
Del Pozo
E
E
Baeyens
J M
JM
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D004305:Dose-Response Relationship, Drug; D005260:Female; D051379:Mice; D009020:Morphine / Q000037:antagonists & inhibitors*; D009043:Motor Activity / Q000187:drug effects*; D026902:Potassium Channel Blockers; D013453:Sulfonylurea Compounds / Q000494:pharmacology*
D026902:Potassium Channel Blockers; D013453:Sulfonylurea Compounds; D009020:Morphine; D000255:Adenosine Triphosphate; C010969:gliquidone