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 D1 receptor antagonist SCH 23390 (R-(+)-8-chloro-2,3,4,5-tetrahydro-3-methyl-5-phenyl-1H-3-benzazepine-7-ol maleate) (0.01, 0.05 and 0.1 mg/kg) and the beta-adrenoreceptor antagonist propranolol (10 mg/kg) increased the nicotine response. The dopamine receptor D2 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 alpha-adrenoceptor antagonist phenoxybenzamine (1 and 10 mg/kg) and the peripheral dopamine D2 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.
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ABSTRACT: The abuse liability of nicotine is comparable to or greater than that of a variety of addictive substances. However, the reinforcing and/or rewarding properties of addictive substances other than nicotine far outweigh the reinforcing and/or rewarding effects associated with nicotine use. These data suggest that, in addition to the intrinsic reinforcing effects of nicotine, other factors may contribute to nicotine addiction. One such factor is associative learning, or rather, the ability of nicotine to alter learning and memory processes that may underlie addiction. The present paper presents an overview of the role of learning in nicotine addiction. In addition, recent advances in the identification of behavioral processes, neural substrates, and cellular and molecular substrates that underlie nicotine-associated alterations in learning are reviewed. Particular attention has been paid to research that describes the role of the hippocampus and hippocampus-dependent learning processes in nicotine addiction.Current Drug Abuse Reviews 02/2008; 1(1):9-19.