Complex interactions between nicotine and nonpharmacological stimuli reveal multiple roles for nicotine in reinforcement
Abstract
Rationale Although considerable progress has been made, we do not yet fully understand the behavioral and neurobiological basis of nicotine reinforcement, and without this knowledge, treatment strategies aimed at reducing smoking remain deficient.Objectives This review describes an original perspective on nicotine reinforcement, which arises from substantial evidence of complex interactions between nicotine and nonpharmacological stimuli. We hypothesize that nicotine reinforcement derives from at least two sources: (1) primary reinforcement, an action that requires response-dependent drug administration and is capable of conveying secondary reinforcing effects on associated stimuli, and (2) the reinforcement-enhancing effect of nicotine, which directly enhances behavior maintained by salient nonnicotine stimuli and does not require a contingent relationship between drug administration and reinforced operant responding. Although novel for nicotine, this hypothesis has origins in an extensive literature on the reinforcing effects of psychostimulants. Empirical support for this hypothesis, based largely on animal models of reinforcement, will be presented.Conclusions Animal models of drug reinforcement have evolved to reflect our growing awareness of the multidimensional nature of drug dependence in humans. Investigating the interaction between nicotine and nonpharmacological stimuli within the context of the drug self-administration paradigm in rats has generated new insights into the paradox of how nicotine, an apparently weak primary reinforcer, can sustain the robust behavior observed in self-administration and in smoking. The hypothesis presented in this paper--that nicotine acts as both a primary reinforcer and an enhancer of other nonnicotine reinforcers--provides important direction for future investigations into the neurobiology of nicotine reinforcement and treatments for smoking cessation.
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Both nicotine and bupropion increase responding for reinforcing non-drug stimuli.
“and increase responding for reinforcing non-drug stimuli [229–231].”
From Mechanistic insights into nicotine withdrawal (2011) · cites this paper as [229]
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REVIEW: Behavioural assessment of drug reinforcement and addictive features in rodents: an overview
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Self-citationChaudhri, N., Caggiula, A. R., Donny, E. C., Booth, S., Gharib, M., Craven, L., Palmatier, M. I., Liu, X., & Sved, A. F. (2006) · Psychopharmacology · doi:10.1007/s00213-006-0522-0 · Cited by 123 · see citing works
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Self-citation
- Authors
- Chaudhri, N., Caggiula, A. R., Donny, E. C., Palmatier, M. I., Liu, X., & Sved, A. F.
- Affiliations
- University of Pittsburgh (US)
- Corresponding author
- Chaudhri, Nadia
- Caggiula, Anthony R.
- Venue
- Psychopharmacology
- Published
- 2005-10-21
- Volume
- 184
- Issue
- 3-4
- Pages
- 353-366
- ISSN
- 0033-3158 (ISSN-L)
- 1432-2072
- OpenAlex
- W2106466862
- Cited by
- 271
- References
- 193
- Citations by year
- 2026: 6 · 2025: 6 · 2024: 3 · 2023: 4 · 2022: 6 · 2021: 10 · 2020: 7 · 2019: 12 · 2018: 10 · 2017: 8 · 2016: 18 · 2015: 23 · 2014: 24 · 2013: 14 · 2012: 21
- FWCI
- 1.97
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Psychopharmacology (publishedVersion)
- PubMed (publishedVersion)
- D-Scholarship@Pitt (University of Pittsburgh) (acceptedVersion)
- Funders
- National Institute on Drug Abuse (DA-12655, R01DA010464, DA-10464, R01DA012655)
- 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 reinforcement, primary reinforcement, secondary reinforcement, self-administration, psychostimulants, smoking cessation, drug addiction
- MeSH terms
- Animals, Association Learning, Conditioning, Operant, Cues, Disease Models, Animal, Dose-Response Relationship, Drug, Humans, Motivation, Nicotine, Reinforcement, Psychology, Self Administration, Smoking, Tobacco Use Disorder, Rats
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