The Role of Nicotine in Smoking: A Dual-Reinforcement Model
Open accessAbstract
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 is the principle of primary reinforcement, which posits that response-contingent presentation of a primary reinforcer, nicotine, engenders robust operant behavior, whereas response-independent drug delivery does not. This dictum of nicotine as a primary reinforcer has been widely used to explain why people smoke tobacco-smoking results in the rapid delivery of nicotine to the brain, setting up a cascade of neurobiological processes that strengthen subsequent smoking behavior. However, there is mounting evidence that the primary reinforcement model of nicotine self-administration fails to fully explain existing data from both the animal self-administration and human smoking literatures. We have recently proposed a "dual reinforcement" model to more fully capture the relationship between nicotine and self-administration, including smoking. Briefly, the "dual reinforcement" model posits that nicotine acts as both a primary reinforcer and a reinforcement enhancer. The latter action of nicotine had originally been uncovered by showing that a reinforcing VS, which accompanies nicotine delivery, synergizes with nicotine in the acquisition and maintenance of self-administration, and that this synergism can be reproduced by combining operant responding for the reinforcing stimulus with non-contingent (response-independent) nicotine. Thus, self-administration (and smoking) is sustained by three actions: (1) nicotine, acting as a primary reinforcer, can sustain behavior that leads to its delivery; (2) nicotine, acting as a primary reinforcer, can establish neutral environmental stimuli as conditioned reinforcers through Pavlovian associations; and (3) nicotine, acting as a reinforcement enhancer, can magnify the incentive value of accompanying stimuli, be they conditioned or unconditioned reinforcers.
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Drugs such as nicotine produce increases in dopamine transmission but fail to produce any reported 'liking' or euphoria in humans, suggesting the absence of any clear relationship between 'liking' and the excessive 'wanting' that leads to addiction.
“Furthermore, drugs such as nicotine produce increases in dopamine transmission but fail to produce any reported ‘liking’ or euphoria in humans, suggesting the absence of any clear relationship between ‘liking’ and the excessive ‘wanting’ that leads to addiction (Balfour, 2015b; Caggiula et al., 2009; Rose, Behm, Westman, & Johnson, 2000).”
From Cued for Risk: Evidence for an Incentive Sensitization Framework to Explain the Interplay between Stress and Anxiety, Substance Abuse, and Reward Uncertainty in Disordered Gambling Behavior (2019) · cites this paper as Caggiula et al., 2009
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- Authors
- Caggiula, A. R., Donny, E. C., Palmatier, M. I., Liu, X., Chaudhri, N., & Sved, A. F.
- Affiliations
- University of Pittsburgh (US)
- Corresponding author
- Caggiula, Anthony R.
- Venue
- Nebraska Symposium on Motivation
- Publisher
- Springer US
- Published
- 2008
- Volume
- 55
- Pages
- 91-109
- ISSN
- 0146-7875 (ISSN-L)
- PMC
- PMC2694565
- OpenAlex
- W1032732133
- Cited by
- 226
- References
- 62
- Citations by year
- 2026: 4 · 2025: 9 · 2024: 4 · 2023: 9 · 2022: 10 · 2021: 14 · 2020: 7 · 2019: 13 · 2018: 20 · 2017: 15 · 2016: 19 · 2015: 24 · 2014: 28 · 2013: 13 · 2012: 16
- FWCI
- 53.86
- Type
- conference paper
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Nebraska Symposium on Motivation/The Nebraska symposium on motivation (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Drug Abuse (R01DA017288, DA-12655, R01DA010464, DA-10464, DA-17288, R01DA012655, F32DA019278, DA19278)
- Topics
- Health Sciences › Medicine › Physiology › Smoking Behavior and Cessation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nicotinic Acetylcholine Receptors Study
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Keywords
- nicotine, primary reinforcement, nicotine self-administration, conditioned reinforcer, classical conditioning, incentive value, smoking cessation pharmacotherapy
- MeSH terms
- Animals, Association Learning, Conditioning, Psychological, Cues, Disease Models, Animal, Ganglionic Stimulants, Humans, Motivation, Nicotine, Reward, Self Administration, Smoking, Social Environment, Substance Withdrawal Syndrome, Tobacco Use Disorder, Smoking Cessation, Rats
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