Dissociation of physical abstinence signs from changes in extracellular dopamine in the nucleus accumbens and in the prefrontal cortex of nicotine dependent rats
Abstract
The aim of the present study was to investigate the relationship between physical abstinence and changes in dopamine release in the nucleus accumbens and in the medial prefrontal cortex induced by mecamylamine and naloxone in rats chronically exposed to nicotine. The rats were implanted with osmotic minipumps (Alzet) delivering nicotine tartrate at a rate of 9 mg/kg/day (3.16 mg of free base) and 8 days later with a dialysis probe in the nucleus accumbens or in the medial prefrontal cortex. Steady-state dopamine output from the nucleus accumbens of the rats implanted with nicotine minipumps was higher than that of sham implanted rats; no differences were observed in the prefrontal cortex. In nicotine but not in sham implanted rats mecamylamine (1 mg/kg s.c.) precipitated a physical abstinence syndrome and brought dopamine output back to control values in the nucleus accumbens. In contrast mecamylamine (1 mg/kg s.c.) increased dopamine output in the medial prefrontal cortex of nicotine but not sham-implanted rats. Naloxone (2 mg/kg) precipitated a physical abstinence syndrome qualitatively similar to that produced by mecamylamine but failed to modify extracellular dopamine in the nucleus accumbens or in the prefrontal cortex of nicotine-implanted and sham-implanted rats. The results indicate that the mesolimbic and mesocortical dopamine system undergo opposite changes during mecamylamine-precipitated abstinence in rats chronically exposed to nicotine and that physical abstinence signs can be dissociated from changes in dopamine transmission.
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Dopaminergic deficits in the mesolimbic pathway, particularly in the nucleus accumbens, are among the neurochemical mechanisms underlying nicotine withdrawal symptoms.
“Dopaminergic deficits in the mesolimbic pathway, particularly in the nucleus accumbens, are among the neurochemical mechanisms underlying the symptoms of nicotine withdrawal (Hildebrand et al. 1998; Carboni et al. 2000; Rada et al. 2001).”
From Nicotine Withdrawal (2015) · cites this paper as Carboni et al. 2000
During withdrawal, DA transmission deficits in the NAcc are paralleled by increased DA output in the PFC.
“Interestingly, the deficits in DA transmission observed in the NAcc during withdrawal are paralleled by an increase in DA output in the prefrontal cortex (PFC) [138].”
From Mechanistic insights into nicotine withdrawal (2011) · cites this paper as [138]
Acute withdrawal from major drugs of abuse including nicotine decreases mesolimbic DAergic activity.
“Acute withdrawal from all major drugs of abuse, including nicotine, decreases activity of the mesolimbic DAergic system, [135–139]”
From Mechanistic insights into nicotine withdrawal (2011) · cites this paper as [138]
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- Authors
- Carboni, E., Bortone, L., Giua, C., & Di Chiara, G.
- Affiliations
- University of Cagliari (IT)
- Corresponding author
- Carboni, Ezio
- Venue
- Drug and Alcohol Dependence
- Publisher
- Elsevier BV
- Published
- 2000-02
- Volume
- 58
- Issue
- 1-2
- Pages
- 93-102
- ISSN
- 0376-8716 (ISSN-L)
- OpenAlex
- W2025491101
- Cited by
- 96
- References
- 40
- Citations by year
- 2025: 2 · 2023: 1 · 2022: 1 · 2021: 1 · 2020: 1 · 2019: 1 · 2018: 1 · 2016: 3 · 2015: 3 · 2014: 7 · 2013: 3 · 2012: 4
- FWCI
- 3.47
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Drug and Alcohol Dependence (publishedVersion)
- PubMed (publishedVersion)
- UNICA IRIS Institutional Research Information System (University of Cagliari) (submittedVersion)
- Funders
- European Commission
- Topics
- Health Sciences › Medicine › Physiology › Smoking Behavior and Cessation
- 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
- Keywords
- nicotine dependence, extracellular dopamine, nucleus accumbens, medial prefrontal cortex, mecamylamine, naloxone, mesolimbic dopamine system, mesocortical dopamine system, nicotine self-administration, nicotine withdrawal
- MeSH terms
- Analysis of Variance, Animals, Behavior, Animal, Dopamine, Male, Mecamylamine, Naloxone, Narcotic Antagonists, Nicotine, Nucleus Accumbens, Substance Withdrawal Syndrome, Infusion Pumps, Implantable, Rats, Sprague-Dawley, Prefrontal Cortex, Nicotinic Antagonists, Rats
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