Effects of monoamine receptor antagonists on nicotine-induced hypophagia in the rat

(--)-Nicotine, in doses of 0.2-0.6 mg/kg intraperitoneally (i.p.), induced a dose-dependent anorexia 1 h, 2 h and 4 h after food presentation in 20-h food-restricted male rats. The anorectic response of nicotine (0.4 mg/kg, 30 min before the test) was prevented by pretreatment with the central nicotine receptor antagonist mecamylamine (0.5 and 1 mg/kg). The peripheral nicotine receptor antagonist hexamethonium (5 and 10 mg/kg), the muscarinic receptor antagonist atropine (5 and 10 mg/kg), the dopamine D2 receptor antagonist pimozide (0.5 and 1 mg/kg), the dopamine D1 receptor antagonist SCH23390 (R-(+)-8-chloro-2, 3, 4, 5-tetrahydro-3-methyl-5-phenyl-1 H-3-benzazepine-7ol maleate; 0.05 and 0.1 mg/kg), the alpha-adrenoceptor antagonist phenoxybenzamine (5 and 10 mg/kg), and the beta-adrenoceptor antagonist propranolol (5 and 10 mg/kg) amplified the nicotine response while promoting anorexia by themselves. The dopamine D2 receptor antagonist sulpiride (25, 50 and 100 mg/kg) increased food intake and amplified the anorectic effect of nicotine. The 5-HT receptor antagonists metergoline (0.5 and 1 mg/kg) and mianserin (1 and 2 mg/kg) increased the nicotine effect. When the antagonists were used alone, metergoline did not change food intake, while mianserin increased food intake. It can be concluded that part of nicotine-induced anorexia is mediated through central nicotinic receptors.