Central mechanisms for apomorphine-induced emesis in the dog.

Abstract In order to investigate whether different receptor populations mediate emesis induced by intracerebroventricular (i.c.v.) and intravenous (i.v.) apomorphine, adult beagle dogs were tested with various doses of the drug with and without central and peripheral pretreatment with the dopamine antagonist sulpiride. The threshold dose of apomorphine to induce emesis by i.c.v. injections was 30–50 times lower than via the i.v. route, while the response latencies after i.c.v. administration were typically longer and the number of bouts of vomiting greater. I.v. pretreatment with sulpiride was more effective than i.c.v. pretreatment in blocking emesis induced by i.v. apomorphine, whereas both i.v. and i.c.v. sulpiride effectively blocked vomiting after i.c.v. apomorphine. Finally, in separate experiments, surgical interruption of blood flow in the region of the area postrema permanently abolished the emetic response to i.c.v. apomorphine, but only transiently disrupted emesis induced by i.v. apomorphine. These data suggest the possibility that i.v. and i.c.v. apomorphine-induced emesis may be mediated by separate dopamine receptors on the cerebrospinal fluid-side and blood-side of the area postrema.