Decreased Signs of Nicotine Withdrawal in Mice Null for the β4 Nicotinic Acetylcholine Receptor Subunit
Open accessAbstract
Withdrawal from chronic exposure to nicotine, the main addictive component of tobacco, produces distinctive symptoms in humans. The appearance of these symptoms is a major deterrent when people try to quit smoking. To study which type of nicotine receptor is relevant for the onset of the withdrawal syndrome, we used a mouse model of nicotine withdrawal. Wild-type mice and mice null for the β4 (β4-/-) or the β2 (β2-/-) nicotinic acetylcholine receptor subunits were implanted with osmotic minipumps delivering 24 mg · kg -1 · d -1 nicotine for 13 d. Subsequently, a single intraperitoneal injection of the nicotinic receptor antagonist mecamylamine induced behavioral symptoms of withdrawal measured as increased grooming, chewing, scratching, and shaking, plus the appearance of some unique behaviors such as jumping, leg tremors, and cage scratching. Mecamylamine injection triggered comparable withdrawal signs in wild-type and in β2-/- mice, whereas the β4-/- mice displayed significantly milder somatic symptoms. In addition, nicotine withdrawal produced hyperalgesia in wild-type but not β4-/- mice. Finally, chronic nicotine produced an increase in epibatidine binding in several areas of the brain in both wild-type and in β4-/- mice, but such receptor upregulation did not correlate with the severity of withdrawal signs. Our results demonstrate a major role for β4-containing nicotinic acetylcholine receptors in the appearance of nicotine withdrawal symptoms. In contrast, the β2 subunit does not seem to greatly influence this phenomenon. We also show that the upregulation of epibatidine binding sites attributable to chronic nicotine, an effect associated with β2-containing receptors, is probably not related to the mechanisms underlying withdrawal.
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β4 knockout mice show no somatic signs of nicotine withdrawal or hyperalgesia after mecamylamine-precipitated withdrawal.
“β4 KO mice exhibit no somatic signs of nicotine withdrawal or hyperalgesia following mecamylamine-induced withdrawal (Salas et al. 2004).”
From Nicotine Withdrawal (2015) · cites this paper as Salas et al. 2004
The Results section reports fewer somatic signs in nicotine-treated β4 knockout mice after mecamylamine, not no signs. It also reports no hyperalgesia in β4 knockout mice, but the Animals section specifies that the hyperalgesia tests were performed after interruption of nicotine infusion, rather than after mecamylamine-precipitated withdrawal. Page numbers are not provided in the supplied copy. (LLM, conf=0.94)
Experimental — accuracy not yet measuredβ2 knockout mice have somatic withdrawal signs and abstinence-induced hyperalgesia comparable to wild-type mice.
“β2 KO mice exhibit levels of somatic signs of withdrawal and abstinence-induced hyperalgesia comparable to those of WT mice (Salas et al. 2004).”
From Nicotine Withdrawal (2015) · cites this paper as Salas et al. 2004
The Results section reports that β2 knockout mice had somatic withdrawal scores similar to nicotine-treated controls after mecamylamine injection. Its hyperalgesia results compare wild-type mice with β4 knockout mice, not β2 knockout mice, so the claimed comparison of abstinence-induced hyperalgesia is not supported (page not specified in our copy). (LLM, conf=0.88)
Experimental — accuracy not yet measuredSomatic signs of withdrawal are preserved in mice lacking β2 or α6 nAChR subunits.
“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 [11]
Absence of α2, α5, or β4 nAChR subunits abolishes somatic manifestations of nicotine withdrawal.
“The MHb/IPN express nAChRs comprising the α2 (IPN), α5, and/or β4 nAChR subunits and absence of any one of those nAChR subunits abolishes the somatic manifestations of nicotine withdrawal [11, 81, 170].”
From Mechanistic insights into nicotine withdrawal (2011) · cites this paper as [11]
Rodents chronically exposed to nicotine undergo a characteristic withdrawal syndrome that can occur spontaneously or be precipitated by mecamylamine.
“Rodents chronically exposed to nicotine undergo a characteristic withdrawal syndrome which develops spontaneously, after removing the nicotine source, or can be precipitated by administration of a nAChR antagonist such as mecamylamine [7, 11, 81, 163–166].”
From Mechanistic insights into nicotine withdrawal (2011) · cites this paper as [11]
Varenicline's interactions with α3β4-, α2-, or α6-containing nAChRs might contribute to its therapeutic effects.
“Varenicline’s interactions with α3β4-, α2-, or α6-containing nAChRs might also contribute to its therapeutic effects given the role of those receptors in both the rewarding and/or aversive effects of nicotine [11, 13, 80, 81].”
From Mechanistic insights into nicotine withdrawal (2011) · cites this paper as [11]
The MHb/IPN axis is emerging as a brain circuit involved in processing anti-reward stimuli and nicotine withdrawal.
“which, as discussed in section 2.3, is emerging as a brain circuit involved in the processing of anti-reward stimuli and nicotine withdrawal [11, 80, 222].”
From Mechanistic insights into nicotine withdrawal (2011) · cites this paper as [11]
Not all withdrawal symptoms are mediated by β2* nAChRs; β4*, α5*, and α7 nAChRs, but not β2* nAChRs, contribute to somatic withdrawal symptoms.
“not all withdrawal symptoms are mediated by β2* nAChRs; for example, β4*, α5*, and α7 nAChRs, but not β2* nAChRs, contribute to somatic withdrawal symptoms (Jackson et al., 2008; Salas et al., 2007; Salas et al., 2004).”
From The duration of nicotine withdrawal-associated deficits in contextual fear conditioning parallels changes in hippocampal high affinity nicotinic acetylcholine receptor upregulation (2012) · cites this paper as Salas et al., 2004
SePhaChARNS probably does not explain withdrawal.
“SePhaChARNS probably does not explain withdrawal (13,14),”
From Nicotine is a selective pharmacological chaperone of acetylcholine receptor number and stoichiometry. Implications for drug discovery (2009) · cites this paper as [13]
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- Authors
- Salas, R., Pieri, F., & De Biasi, M.
- Affiliations
- Baylor College of Medicine (US)
- ORCID
- Salas, Ramiro
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2004-11-10
- Volume
- 24
- Issue
- 45
- Pages
- 10035-10039
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC6730195
- OpenAlex
- W1989152115
- Cited by
- 226
- References
- 36
- Citations by year
- 2025: 3 · 2024: 3 · 2023: 7 · 2022: 2 · 2021: 5 · 2020: 13 · 2019: 7 · 2018: 9 · 2017: 11 · 2016: 13 · 2015: 21 · 2014: 26 · 2013: 16 · 2012: 13
- FWCI
- 2.47
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute on Drug Abuse (DA017173, R01DA017173)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nicotinic Acetylcholine Receptors Study
- Health Sciences › Medicine › Physiology › Smoking Behavior and Cessation
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- nicotine withdrawal, nicotinic acetylcholine receptors, beta4 subunit, beta2 subunit, mecamylamine, epibatidine binding, chronic nicotine exposure, hyperalgesia, receptor up-regulation, smoking cessation, mouse model
- MeSH terms
- Animals, Behavior, Animal, Female, Genotype, Grooming, Hyperalgesia, Male, Mastication, Mecamylamine, Mice, Inbred C57BL, Nerve Tissue Proteins, Nicotine, Pyridines, Receptors, Nicotinic, Substance Withdrawal Syndrome, Tremor, Infusion Pumps, Implantable, Mice, Knockout, Bridged Bicyclo Compounds, Heterocyclic, Mice
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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