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The Role of α6-Containing Nicotinic Acetylcholine Receptors in Nicotine Reward and Withdrawal
Open accessAbstract
The alpha6 nicotinic acetylcholine receptor (nAChR) subunit is involved in nicotine-stimulated dopamine release in the striatum. It is expressed in brain regions and coexpressed with nAChR subtypes implicated in nicotine dependence behaviors; hence, this subunit may play a role in nicotine dependence. Using the alpha6-selective antagonist alpha-conotoxin H9A;L15A (MII[H9A;L15A]), we determined the role of alpha6* nAChRs in the pharmacological and behavioral effects of nicotine. We measured effects of pretreatment with MII[H9A;L15A] on analgesia, locomotion, and body temperature after a single injection of nicotine. Effects of MII[H9A;L15A] on nicotine reward were measured using the conditioned place preference (CPP) paradigm. We further measured physical (somatic signs and hyperalgesia) and affective [anxiety-related behavior and conditioned place aversion (CPA)] nicotine withdrawal behaviors after extended nicotine exposure. Results showed that MII[H9A;L15A] did not block acute nicotine effects on the behaviors measured. Conversely, MII[H9A:l15A] blocked the expression of nicotine CPP, as well as withdrawal-associated CPA and anxiety-related behavior in the elevated plus maze, but not withdrawal-induced somatic signs or hyperalgesia. These results suggest a role for the alpha6 nAChR subunit in nicotine reward and affective nicotine withdrawal but not acute nicotine-induced or physical withdrawal behaviors.
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“There was no influence on the somatic symptoms of withdrawal, suggesting a selective role for α6 nAChR subunits in the affective manifestations of withdrawal (Jackson et al. 2009).”
From Nicotine Withdrawal (2015) · cites this paper as Jackson et al. 2009
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“and there is a documented role for α6* nAChRs in withdrawal-induced CPA (Jackson et al. 2009).”
From Nicotine Withdrawal (2015) · cites this paper as Jackson et al. 2009
In the citing paper
“Pharmacological studies in nAChR null mice indicate that β2-containing and α6-containing nAChRs are necessary for CPA, but neither the α5, nor the α7 subunits affect CPA behavior [170, 172, 189].”
From Mechanistic insights into nicotine withdrawal (2011) · cites this paper as [172]
In the citing paper
“Interestingly, somatic signs of withdrawal are preserved in mice lacking the β2 or the α6 nAChR subunits [11, 172]”
From Mechanistic insights into nicotine withdrawal (2011) · cites this paper as [172]
In the citing paper
“So far, it has been established that the β2 and α6 nAChR subunits are necessary for increased anxiety during withdrawal [170, 172], whereas, α5 and α7 may not be required [170].”
From Mechanistic insights into nicotine withdrawal (2011) · cites this paper as [172]
In the citing paper
“In addition, infusion and systemic administration of drugs that selectively inhibit ␣42* and/or ␣62* nAChRs blocked behaviors linked to nicotine reward and reinforcement”
From Varenicline Is a Potent Partial Agonist at α6β2* Nicotinic Acetylcholine Receptors in Rat and Monkey Striatum (2012) · cites this paper as Jackson et al., 2009
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Metadata
- Authors
- Jackson, K. J., McIntosh, J. M., Brunzell, D. H., Sanjakdar, S. S., & Damaj, M. I.
- Affiliations
- Virginia Commonwealth University (US)
- Venue
- The Journal of Pharmacology and Experimental Therapeutics
- Publisher
- Elsevier BV
- Published
- 2009-11
- Volume
- 331
- Issue
- 2
- Pages
- 547-554
- ISSN
- 0022-3565 (ISSN-L)
- PMC
- PMC2775251
- OpenAlex
- W2133971381
- Cited by
- 135
- References
- 38
- Citations by year
- 2026: 2 · 2025: 3 · 2024: 3 · 2023: 8 · 2022: 3 · 2021: 2 · 2020: 8 · 2019: 7 · 2018: 6 · 2017: 8 · 2016: 8 · 2015: 15 · 2014: 17 · 2013: 13 · 2012: 14
- FWCI
- 4.29
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Pharmacology and Experimental Therapeutics (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (MH53631, GM 48677)
- National Institute of Mental Health (MH53631, R01MH053631, R29MH053631)
- National Institute on Drug Abuse (R01DA012610, DA 05274, DA-12610, R03DA023114, DA023114, P50DA005274)
- National Institute of General Medical Sciences (P01GM048677, GM48677)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nicotinic Acetylcholine Receptors Study
- Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Smoking Behavior and Cessation
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Keywords
- nicotine reward, nicotine withdrawal, conditioned place preference, conditioned place aversion, anxiety-like behavior, nicotine dependence, dopamine release, striatum, hyperalgesia, locomotion, analgesia, body temperature
- MeSH terms
- Animals, Anxiety, Avoidance Learning, Body Temperature, Calcium Channel Blockers, Conditioning, Operant, Dose-Response Relationship, Drug, Injections, Intraventricular, Male, Mice, Inbred C57BL, Motor Activity, Nicotine, Pain Measurement, Reaction Time, Receptors, Nicotinic, Reward, Substance Withdrawal Syndrome, Nicotinic Agonists, Nicotinic Antagonists, Conotoxins, Mice
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