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pubmed-article:17229101pubmed:abstractTextAlthough nicotine is considered to be responsible for the addictive properties of tobacco, growing evidence underlines the importance of non-nicotine components in smoking reinforcement. It has been shown that tobacco smoke contains monoamine oxidase (MAO) A and B inhibitors and decreases MAO-A and MAO-B activity in smokers. Here, we investigated the effects of clorgyline hydrochloride (irreversible MAO-A inhibitor; 2 mg/kg/day), selegiline (irreversible MAO-B inhibitor; 4 mg/kg) and the beta-carboline norharmane hydrochloride (reversible MAO-B inhibitor; 5 mg/kg/day) treatments on nicotine self-administration (30 microg/kg/infusion, free base) in rats. Independent of the responsiveness to novelty and locomotor activity stimulation, only clorgyline hydrochloride treatment increased the intake of nicotine in a fixed-ratio schedule (FR5) of reinforcement. When a progressive-ratio schedule was implemented, both clorgyline hydrochloride and norharmane hydrochloride treatments potentiated the reinforcing effects of nicotine, whereas selegiline had no effect. Taken together, these results indicate that MAO-A inhibition interacts with nicotine to enhance its rewarding effects in rats and suggest that other compounds present in tobacco, such as beta-carboline, may also play an important role in sustaining smoking behavior in humans.lld:pubmed
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pubmed-article:17229101pubmed:articleTitleMonoamine oxidase A rather than monoamine oxidase B inhibition increases nicotine reinforcement in rats.lld:pubmed
pubmed-article:17229101pubmed:affiliationLaboratoire de Neuropsychobiologie des Désadaptations, UMR CNRS 5541, Université de Bordeaux 2, BP 31, 146 rue Léo Saignat, 33076 Bordeaux, cedex, France.lld:pubmed
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pubmed-article:17229101pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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