Effects of nicotine on memory retrieval in mice

Abstract

The effect of nicotine was tested on retrieval 24 h after training on a passive avoidance task. Intraperitoneal (i.p.) injection of nicotine (0.25–1.5 mg/kg) increased the step-down latency in mice dose dependently. Pretreatment with the nicotinic receptor antagonist mecamylamine (0.5–1 mg/kg) decreased, whereas pretreatment with the dopamine D 1 receptor antagonist SCH 23390 ( R-(+)-8-chloro-2,3,4,5-tetrahydro-3-methyl-5-phenyl-1 H-3-benzazepine-7-ol maleate) (0.01, 0.05 and 0.1 mg/kg) and the β-adrenoreceptor antagonist propranolol (10 mg/kg) increased the nicotine response. The dopamine receptor D 2 receptor antagonist sulpiride (5–10 mg/kg), the anti-muscarinic agent atropine (2.5–10 mg/kg), the peripheral nicotinic receptor antagonist hexamethonium (0.01–0.5 mg/kg), the α-adrenoceptor antagonist phenoxybenzamine (1 and 10 mg/kg) and the peripheral dopamine D 2 receptor antagonist domperidone (5 and 10 mg/kg) did not change the response induced by nicotine. Single administration of the antagonists did not cause response; however, a high dose of domperidone (10 mg/kg) and propranolol alone increased the step-down latencies. It may be concluded that a nicotinic receptor mechanism is involved in the nicotine-induced improvement of memory retrieval.