Nicotine, Tobacco Use, and the 55th Nebraska Symposium on Motivation

Tobacco use is a worldwide health problem. As so well stated by Mackay and Ericksen (2002), “No other consumer product is as dangerous, or kills as many people. Tobacco kills more than AIDS, legal drugs, illegal drugs, road accidents, murder, and suicide combined” (p. 36). Imagine the lives saved, and the amount of pain, emotional suffering, and fiscal burden alleviated, if we could devise approaches that helped current tobacco users quit and remain abstinent, and prevented new smokers from emerging. Although these idealistic goals are worth pursuing, improving cessation rates by only a small fraction, or making small gains in preventing people from experimenting with tobacco, would nevertheless translate into significant improvement in the health and well-being of countless thousands worldwide as well as financial savings to employers, government institutions, and the heath care system. Even such small, incremental steps require a concerted and coordinated effort by basic scientists, clinical researchers and practitioners, and policy makers to discover the basis of tobacco dependence and apply that knowledge to the implementation of prevention policies and smoking cessation aids. This year\u27s Nebraska Symposium on Motivation was devoted to research on the drug that is widely believed to form the basis of tobacco use and dependence, nicotine

Differentiating the Primary Reinforcing and Reinforcement-Enhancing Effects of Varenicline

Rationale: Varenicline (VAR), a smoking cessation aid that is a partial agonist at nicotinic receptors, mimics the reinforcement-enhancing effects of nicotine. Varenicline, when accompanied by non-drug cues, is self-administered by rats, though it is unclear whether this results from varenicline acting as a primary reinforcer or a reinforcement enhancer of the cues. Objectives: This study sought to disentangle these two potential actions. Methods: Rats were allowed to self-administer intravenous nicotine, saline, or varenicline during 1-h sessions in operant chambers equipped with two levers. Five groups had concurrent access to drug infusions and a moderately reinforcing visual stimulus (VS) for responding on separate levers. Meeting the reinforcement schedule on one lever was reinforced with VAR (0.01, 0.06, 0.1 mg/kg/infusion), nicotine (0.06 mg/kg/infusion), or saline, while meeting the same schedule on the other lever delivered the VS. Additional groups were reinforced for pressing a single active lever and received VAR paired with the VS, the VS with response-independent infusions of VAR, or VAR alone (0.1 mg/kg/infusion). Results: Rats readily responded for VAR paired with VS on a single lever. However, when VAR was the only reinforcer contingent on a response, rats did not respond more than for saline. Conclusions: These findings show that VAR does not serve as a primary reinforcer in rats at doses that increase responding for non-drug reinforcers. These data are consistent with research showing that the primary reinforcing effects of VAR are weak, at best, and that the primary reinforcing and reinforcement-enhancing actions of nicotinic drugs are pharmacologically distinct