Nicotine-induced purposeless chewing in rats: possible dopamine receptor mediation

Abstract

Intraperitoneal (i.p.) administration of nicotine to rats induced purposeless chewing. The response induced by different doses of the drug (0.0001, 0.001, 0.01 and 0.1 mg/kg) seems to be dose dependent, with a maximum effect at 0.01 mg/kg and then decreasing at a higher dose (0.1 mg/kg). Pre-treatment of animals with the nicotine antagonist mecamylamine (0.01 and 0.1 mg/kg, 30 min) and the D-2 receptor antagonist sulpiride (12.5-100 mg/kg, 90 min), but not the D-1 antagonist SCH 23390 (0.01 and 0.05 mg/kg, 30 min), decreased the chewing induced by nicotine (0.01 mg/kg). When animals were pre-treated with propranolol (5 and 10 mg/kg) 60 min, reserpine (2.5 mg/kg) 18 h or α-methyl-p-tyrosine (α-MPT; 250 mg/kg) 60 min before nicotine, the effect of the drug was reduced. However, reserpine (2.5 mg/kg) at 18 h plus α-MPT (250 mg/kg) 60 min prior to nicotine completely inhibited the drug response. Pre-treatment of animals with phenoxybenzamine (2.5 and 5 mg/kg i.p., 60 min) or atropine (5 and 10 mg/kg) did not change the nicotine response significantly. It is concluded that nicotine- induced purposeless chewing is mediated through dopaminergic and nicotinic mechanisms.