Dimethylphenylpiperazinium-induced vomiting: nicotinic mediation in area postrema

In unanesthetized cats the emetic action of dimethylphenylpiperazinium (DMPP) was investigated, after it was injected into the cerebral ventricles through chronically implanted cannulae. DMPP injected in 0.2-2.0 mg doses into the cerebral ventricle produced dose-dependent vomiting, which was abolished after ablation of area postrema. However, copper sulfate given intragastrically evoked vomiting in cats with an ablated area postrema. Further, the emetic response to ICV DMPP and to intragastric copper sulfate was depressed or abolished in cats pretreated with ICV reserpine. The emetic response to ICV DMPP, but not that caused by intragastric copper sulfate, was potentiated in cats pretreated with ICV 5,6-dihydroxytryptamine. Ganglionic blocking agents, mecamylamine and hexamethonium, injected ICV prevented the vomiting elicited by ICV DMPP. On the other hand, selected anti-muscarinic drugs, alpha and beta adrenergic antagonists, dopamine antagonists, antihistamines and a 5-hydroxytryptamine (5-HT) antagonist all injected into the cerebral ventricles had virtually no effect on the vomiting induced by DMPP. It is postulated that DMPP evokes vomiting by its action on nicotinic receptors of nerve cells within the area postrema but not on catecholaminergic, serotonergic, or cholinergic receptors. Finally, 5-HT and acetylcholine could also be involved in the inhibition of the complex mechanisms underlying the central regulation of vomiting.