The α3β4* nicotinic acetylcholine receptor subtype mediates nicotine reward and physical nicotine withdrawal signs independently of the α5 subunit in the mouse
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The 15q25 gene cluster contains genes that code for the α5, α3, and β4 nicotinic acetylcholine receptor (nAChRs) subunits, and in human genetic studies, has shown the most robust association with smoking behavior and nicotine dependence to date. The limited available animal studies implicate a role for the α5 and β4 nAChR subunits in nicotine dependence and withdrawal; however studies focusing on the behavioral role of the α3β4* nAChR receptor subtype in nicotine dependence are lacking. Because of the apparent role of the α3β4* nAChR subtype in nicotine dependence, the goal of the current study was to better evaluate the involvement of this subtype in nicotine mediated behavioral responses. Using the selective α3β4* nAChR antagonist, α-conotoxin AuIB, we assessed the role of α3β4* nAChRs in acute nicotine, nicotine reward, and physical and affective nicotine withdrawal. Because α5 has also been implicated in nicotine dependence behaviors in mice and can form functional receptors with α3β4*, we also evaluated the role of the α3β4α5* nAChR subtype in nicotine reward and somatic nicotine withdrawal signs by blocking the α3β4* nAChR subtype in α5 nAChR knockout mice with AuIB. AuIB had no significant effect on acute nicotine behaviors, but dose-dependently attenuated nicotine reward and physical withdrawal signs, with no significant effect in affective withdrawal measures. Interestingly, AuIB also attenuated nicotine reward and somatic signs in α5 nAChR knockout mice. This study shows that α3β4* nAChRs mediate nicotine reward and physical nicotine withdrawal, but not acute nicotine behaviors or affective nicotine withdrawal signs in mice. The α5 subunit is not required in the receptor assembly to mediate these effects. Our findings suggest an important role for the α3β4* nAChR subtype in nicotine reward and physical aspects of the nicotine withdrawal syndrome.
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α3β4* nAChRs are the most likely contributors to physical components of nicotine withdrawal, given high α3 and β4 mRNA expression in the MHb and the ability of α-conotoxin AuIB to block somatic withdrawal signs.
“α3β4* nAChRs are the most likely contributors to physical components of withdrawal given the high levels of expression of α3 and β4 mRNA in the MHb, and the fact that the α3β4-selective α-conotoxin AuIB blocks the emergence of somatic signs of withdrawal (Jackson et al. 2013).”
From Nicotine Withdrawal (2015) · cites this paper as Jackson et al. 2013
The Results (section 3.4; page unavailable) report that AuIB dose-dependently reduced somatic signs of nicotine withdrawal, and the Discussion (section 4; page unavailable) links α3β4* receptors to physical withdrawal and notes high α3 and β4 subunit expression in the MHb. The copy does not specify that this expression is mRNA expression, and it says α5 receptors also mediate somatic signs; it therefore does not establish α3β4* receptors as the most likely contributors relative to other receptors. (LLM, conf=0.84)
Experimental — accuracy not yet measuredPharmacological evidence indicates that receptors containing α3 and β4 subunits affect both nicotine reward and somatic withdrawal signs.
“pharmacological data suggest that receptors comprising the α3 and β4 nAChR subunits influence both nicotine reward and somatic manifestations of withdrawal (Jackson et al. 2013).”
From Nicotine Withdrawal (2015) · cites this paper as Jackson et al. 2013
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- Authors
- Jackson, K. J., Sanjakdar, S. S., Muldoon, P. P., McIntosh, J. M., & Damaj, M. I.
- Affiliations
- Virginia Commonwealth University (US)
- University of Utah (US)
- Corresponding author
- Damaj, M. Imad
- Venue
- Neuropharmacology
- Publisher
- Elsevier BV
- Published
- 2013-07
- Volume
- 70
- Pages
- 228-235
- ISSN
- 0028-3908 (ISSN-L)
- PMC
- PMC3644352
- OpenAlex
- W1997910583
- Cited by
- 69
- References
- 50
- Citations by year
- 2026: 5 · 2025: 3 · 2024: 2 · 2023: 3 · 2022: 4 · 2021: 4 · 2020: 6 · 2019: 4 · 2018: 3 · 2017: 9 · 2016: 3 · 2015: 12 · 2014: 6 · 2013: 5
- FWCI
- 3.88
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Neuropharmacology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Drug Abuse (R01DA012610, DA-12610)
- 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 › Neurotransmitter Receptor Influence on Behavior
- Keywords
- nicotinic acetylcholine receptors, nicotine reward, nicotine withdrawal, nicotine dependence
- MeSH terms
- Animals, Dose-Response Relationship, Drug, Male, Nicotine, Receptors, Nicotinic, Reward, Substance Withdrawal Syndrome, Mice, Knockout, Nicotinic Agonists, Nicotinic Antagonists, Conotoxins, Mice
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