Effects of cholecystokinin octapeptide on striatal dopamine metabolism and on apomorphine-induced stereotyped cage-climbing in mice.
The effects of sulfated (CCK-8-SE) and non-sulfated (CCK-8-NS) cholecystokinin octapeptide on striatal dopamine (DA) metabolism have been investigated on mice. CCK-8-NS facilitated the disappearance of striatal DA, measured after synthesis inhibition with 350 mg/kg of alpha-methyl-p-tyrosine. CCK-8-SE did not affect DA disappearance. In vitro uptake of [3H]DA by striatal slices was affected by neither CCK-8-SE, nor CCK-8-NS (10(-5) M). Potassium-induced in vitro release of [3H]DA from striatal slices was significantly increased by 10(-5) M CCK-8-NS: however, CCK-8-SE likewise increased DA release in this model system. Apomorphine-induced (1.0 mg/kg) stereotyped cage-climbing behavior was not affected by CCK-8-SE but was enhanced by CCK-8-NS. This effect could be antagonized by haloperidol, but not by naloxone. The data suggest that CCK-8-NS affects striatal DA release, disappearance and receptor sensitivity in the mouse. Dopaminergic mechanisms should therefore be regarded as a possible mode of action of CCK-8-NS on brain functions.
D000818:Animals; D001058:Apomorphine / Q000494:pharmacology*; D002766:Cholecystokinin / Q000031:analogs & derivatives* / Q000494:pharmacology; D003342:Corpus Striatum / Q000378:metabolism*; D004298:Dopamine / Q000378:metabolism*; D004347:Drug Interactions; D006220:Haloperidol / Q000494:pharmacology; D006801:Humans; D008297:Male; D008781:Methyltyrosines / Q000494:pharmacology; D051379:Mice; D009270:Naloxone / Q000494:pharmacology; D011954:Receptors, Dopamine / Q000378:metabolism; D012844:Sincalide; D013239:Stereotyped Behavior / Q000187:drug effects*; D019805:alpha-Methyltyrosine
D008781:Methyltyrosines; D011954:Receptors, Dopamine; D009270:Naloxone; D019805:alpha-Methyltyrosine; D002766:Cholecystokinin; D006220:Haloperidol; D012844:Sincalide; D001058:Apomorphine; D004298:Dopamine