Cited by 740Neurotransmitter Receptor Influence on BehaviorNicotinic Acetylcholine Receptors StudySmoking Behavior and Cessation

Self-administered nicotine activates the mesolimbic dopamine system through the ventral tegmental area

Corrigall, William A., Coen, Kathleen M., Adamson, K. Laurel·1994·Brain Research

Abstract

Microinfusions of the nicotinic antagonist dihydro-beta-erythroidine (DH beta E) were used to examine the role of the mesolimbic dopamine system in nicotine reinforcement in rats. Infusions of DH beta E into the ventral tegmental area (VTA) prior to the start of i.v. nicotine self-administration sessions resulted in a significant decrease in the number of nicotine infusions voluntarily obtained. In contrast, the same doses of DH beta E infused into the nucleus accumbens were without effect on nicotine self-administration. The reductions caused by DH beta E were specific to nicotine reinforcement; neither operant responding maintained by food, cocaine self-administration, or spontaneous locomotor activity were altered by local applications of DH beta E within the VTA. The reduction in nicotine self-administration following treatment in the VTA was also specific to the nicotinic antagonist, and was not duplicated by infusions of the muscarinic antagonist atropine. Partial lesions of the pedunculopontine tegmental nucleus, the likely origin of cholinergic fibers to the VTA, were without effect on nicotine self-administration, suggesting that the effects of DH beta E were not due to disruption of a tonically active cholinergic input to the VTA from this source. These data show that nicotine acts within the VTA region to initiate processes which are critical to the reinforcing properties of the drug.

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Crossref · 10.1016/0006-8993(94)90401-4

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39 of 39 references verified0 citation errors · 0 not checkable

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  • Lesions of the VTA and its primary projection area, the NAc, greatly attenuate nicotine self-administration and the psychostimulant properties of nicotine.

    “Lesions of the ventral tegmental area (VTA) and its primary projection area, the nucleus accumbens (NAc), greatly attenuate nicotine self-administration and the psychostimulant properties of nicotine”

    From Mechanisms of Nicotine Addiction (2021) · cites this paper as Corrigall et al. 1994

  • Both β2* and α7 nAChR subtypes contribute to nicotine-associated increases in DA release and associated nicotine-dependent behaviors.

    “An accumulation of data suggests that both the β2* and α7 nAChR subtypes contribute to nicotine-associated increases in DA release and associated nicotine-dependent behaviors (Corrigall et al., 1994; Epping-Jordan et al., 1999; Laviolette and van der Kooy, 2003; Mansvelder et al., 2002; Picciotto et al., 1998; Pidoplichko et al., 2004; Shoaib and Stolerman, 1994).”
  • Drugs that selectively inhibit α4β2* and/or α6β2* nAChRs block behaviors linked to nicotine reward and reinforcement when infused or given systemically.

    “In addition, infusion and systemic administration of drugs that selectively inhibit ␣4␤2* and/or ␣6␤2* nAChRs blocked behaviors linked to nicotine reward and reinforcement”
  • Disruption of PPTg activity decreases the rewarding and locomotor effects of drugs of abuse such as cocaine and nicotine.

    “At the behavioral level, this conclusion is consistent with the finding that disruption of PPTg activity decreases the rewarding and locomotor effects of drugs of abuse such as cocaine and nicotine (Champtiaux et al., 2006; Corrigall et al., 1994; Corrigall et al., 2002), while lesion of NAc cholinergic neurons increases cocaine self-administration, as might be expected if a pause in cholinergic”
  • The mesolimbic system is preferentially active during exposure to rewards, with the primary consequence being the release of the neurotransmitter dopamine.

    “While these rewards typically all generate pleasure, a vast body of evidence, in both rodents and humans, suggests that the mesolimbic system is preferentially active during exposure to rewards, with the primary consequence being the release of the neurotransmitter dopamine (Balfour, 2015a; Berridge & Robinson, 1998; Corrigall, Coen, & Adamson, 1994; Di Chiara & Imperato, 1988).”

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Authors
Corrigall, W. A., Coen, K. M., & Adamson, K. L.
Affiliations
University of Toronto (CA)
Corresponding author
Corrigall, William A.
Venue
Brain Research
Publisher
Elsevier BV
Published
1994-08
Volume
653
Issue
1-2
Pages
278-284
ISSN
0006-8993 (ISSN-L)
OpenAlex
W2083076890
Cited by
740
References
39
Citations by year
2026: 3 · 2025: 3 · 2024: 6 · 2023: 7 · 2022: 10 · 2021: 8 · 2020: 71 · 2019: 13 · 2018: 21 · 2017: 13 · 2016: 22 · 2015: 15 · 2014: 25 · 2013: 28 · 2012: 25
FWCI
5.01
Type
journal article
Language
en
Open access
closed
Locations
  • Brain Research (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nicotinic Acetylcholine Receptors Study
  • Health Sciences › Medicine › Physiology › Smoking Behavior and Cessation
Keywords
nicotine self-administration, mesolimbic dopamine system, ventral tegmental area, dihydro-beta-erythroidine, nicotinic antagonists, nicotine reinforcement, nucleus accumbens, pedunculopontine nucleus, cholinergic input, atropine, cocaine self-administration, locomotor activity
MeSH terms
Animals, Atropine, Cocaine, Dihydro-beta-Erythroidine, Dopamine, Food, Limbic System, Male, Microinjections, Motor Activity, Nicotine, Rats, Inbred Strains, Reinforcement, Psychology, Self Administration, Tegmentum Mesencephali, Rats

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