Models of intravenous nicotine self-administration in laboratory animals are being used to investigate the behavioral and neurobiological consequences of nicotine reinforcement, and to aid in the development of novel pharmacotherapies for smoking cessation. Central to these models are the principles of contingency and primary reinforcement, which have been widely used to explain why people smoke tobacco - smoking results in the rapid delivery of nicotine to the brain, the consequences of which are to reinforce smoking behavior. However, there is mounting evidence that the primary reinforcement model of nicotine self-administration fails to fully explain existing data. Two other factors must be taken into account to attain a complete understanding of the contribution of nicotine to smoking. One is the role of environmental stimuli that accompany the intake of nicotine, and that contribute to the overall magnitude of reinforcement afforded to the behavior. In a series of experiments, we have shown that a compound visual stimulus that accompanies nicotine delivery is as important as nicotine in critical aspects of nicotine self-administration. The second factor is based on our recent finding that the non-contingent administration of nicotine is as effective as contingently delivered (self-administered) nicotine in maintaining high levels of operant responding for the compound visual stimulus. This finding suggests that nicotine can function as both a primary reinforcer when experienced contingently, and as an enhancer of the reinforcing properties of other stimuli, which does not require a contingent relationship between drug delivery and reinforced operant behavior. Understanding the independent and combined contribution of these two factors will help resolve paradoxes and contradictions in the literature regarding the role of nicotine reinforcement in nicotine self-administration and smoking. Using a yoked paradigm, which contrasts self-administered drug with non-contingent (yoked) drug, we will ask: (1) Can non-contingent nicotine enhance the reinforcing effects of other stimuli such as conditioned reinforcers and reinforcing drugs such as cocaine? (2) Can the reinforcement-enhancing effects of non-contingent nicotine be demonstrated using multiple measures of reinforcement and incentive motivation? (3) Are the dual actions of NIC -- as a primary reinforcer and an enhancer of the reinforcing properties of other stimuli -- exhibited by other drugs such as cocaine? ? ?
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