ArticleNeuropharmacology2013
The α3β4* nicotinic acetylcholine receptor subtype mediates nicotine reward and physical nicotine withdrawal signs independently of the α5 subunit in the mouse.
Article in Neuropharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
42 citing papers in PubMed, 65 citations in OpenAlex.
- Cytisine-New Challenges of a Well-Known Drug in the Treatment of Nicotine Addiction.Journal of clinical medicine · 2026Review
- An accessory orthosteric ligand binding site in the (α3)Cell reports · 2026Article
- Hippocampal Metabolomics Reveal the Mechanism of α-Conotoxin [S9K]TxID Attenuating Nicotine Addiction.Marine drugs · 2026Article
- Nicotinic acetylcholine receptors in pain modulation.Frontiers in pharmacology · 2026Review
- The influence of stress and social defeat on neurobiological reinforcement mechanisms across reward to withdrawal in nicotine addiction.Psychopharmacology · 2025Review
- L-theanine attenuates nicotine reward and withdrawal signs in mice.Neuroscience letters · 2023Article
- What We Have Gained from Ibogaine: α3β4 Nicotinic Acetylcholine Receptor Inhibitors as Treatments for Substance Use Disorders.Journal of medicinal chemistry · 2023Review
- Fluorescently Labeled α-Conotoxin TxID, a New Probe for α3β4 Neuronal Nicotinic Acetylcholine Receptors.Marine drugs · 2022Article
- Mechanism of interactions between α-conotoxin RegIIA and carbohydrates at the human α3β4 nicotinic acetylcholine receptor.Marine life science & technology · 2022Article
- Tobacco smoke exposure enhances reward sensitivity in male and female rats.Psychopharmacology · 2021Article
- Multidimensional Intersection of Nicotine, Gene Expression, and Behavior.Frontiers in behavioral neuroscience · 2021Article
- α-Conotoxin TxID and [S9K]TxID, α3β4 nAChR Antagonists, Attenuate Expression and Reinstatement of Nicotine-Induced Conditioned Place Preference in Mice.Marine drugs · 2020Article
- Advances in smoking cessation pharmacotherapy: Non-nicotinic approaches in animal models.Neuropharmacology · 2020Review
- Nicotinic acetylcholine receptors and nicotine addiction: A brief introduction.Neuropharmacology · 2020Review
- Article
- Nicotinic Acetylcholine Receptor Accessory Subunits Determine the Activity Profile of Epibatidine Derivatives.Molecular pharmacology · 2020Article
- Differences in mechanisms underlying reinstatement of cigarette smoke extract- and nicotine-seeking behavior in rats.Neuropharmacology · 2020Article
- Neuronal nicotinic acetylcholine receptors mediate ∆Addiction biology · 2020Article
- Insights Into Nicotinic Receptor Signaling in Nicotine Addiction: Implications for Prevention and Treatment.Current neuropharmacology · 2018Review
- Discovery of peptide ligands through docking and virtual screening at nicotinic acetylcholine receptor homology models.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
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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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.