ArticleNeuropharmacology2015
Pharmacological stress is required for the anti-alcohol effect of the α3β4* nAChR partial agonist AT-1001.
Article in Neuropharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
What it found
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.
- The role of nicotinic receptors in alcohol consumption.Pharmacological research · 2023Pooled it
- Nicotinic acetylcholine receptors in pain modulation.Frontiers in pharmacology · 2026Review
- What We Have Gained from Ibogaine: α3β4 Nicotinic Acetylcholine Receptor Inhibitors as Treatments for Substance Use Disorders.Journal of medicinal chemistry · 2023Review
- The role of nicotinic acetylcholine receptors in alcohol-related behaviors.Brain research bulletin · 2020Review
- Activation of nicotinic acetylcholine receptors induces potentiation and synchronization within in vitro hippocampal networks.Journal of neurochemistry · 2020Article
- Anti-stress neuropharmacological mechanisms and targets for addiction treatment: A translational framework.Neurobiology of stress · 2018Review
- Differential regulation of alcohol taking and seeking by antagonism at α4β2 and α3β4 nAChRs.Psychopharmacology · 2018Article
- Highly Selective and Potent α4β2 nAChR Antagonist Inhibits Nicotine Self-Administration and Reinstatement in Rats.Journal of medicinal chemistry · 2017Article
- The α3β4 nAChR partial agonist AT-1001 attenuates stress-induced reinstatement of nicotine seeking in a rat model of relapse and induces minimal withdrawal in dependent rats.Behavioural brain research · 2017Article
- Mechanisms and genetic factors underlying co-use of nicotine and alcohol or other drugs of abuse.The American journal of drug and alcohol abuse · 2017Review
- A key role for the N/OFQ-NOP receptor system in modulating nicotine taking in a model of nicotine and alcohol co-administration.Scientific reports · 2016Article
- Stress-Induced Reinstatement of Drug Seeking: 20 Years of Progress.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2016Review
- Varenicline decreases nicotine but not alcohol self-administration in genetically selected Marchigian Sardinian alcohol-preferring (msP) rats.Drug and alcohol dependence · 2015Article
- Early Life Stress, Nicotinic Acetylcholine Receptors and Alcohol Use Disorders.Brain sciences · 2015Review
- Pharmacotherapy: Quest for the quitting pill.Nature · 2015Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Alcohol and nicotine are often taken together. The mechanisms underlying this frequent co-abuse are not well known. Genetic and pharmacological evidence suggests that the nicotinic acetylcholine receptors (nAChRs) containing the α3 and β4 subunits play a role in alcohol as well as nicotine addiction. AT-1001 is a high affinity α3β4 nAChR partial agonist recently found to block nicotine self-administration and relapse-like behavior in rats. Here, to study the involvement of α3β4 nAChRs in the mechanisms that regulate alcohol abuse we evaluated the effects of AT-1001 on alcohol taking and seeking in Sprague-Dawley rats. AT-1001 reduced operant alcohol self-administration at the highest dose examined (3.0 mg/kg), an effect also observed for food self-administration. A dose of 1.5 mg/kg AT-1001, which had no effect on alcohol or food self-administration, essentially eliminated reinstatement of alcohol seeking induced by yohimbine (0.625 mg/kg) whereas, reinstatement induced by alcohol-associated cues was not altered, nor did AT-1001 induce reinstatement of extinguished self-administration on its own. Finally, AT-1001 showed an anxiolytic activity when measured in the presence or absence of yohimbine stress in the elevated plus maze paradigm. Together, these observations do not support a specific involvement of the α3β4 nAChR in mediating alcohol reward or cue-induced relapse to alcohol seeking but rather indicate that the α3β4 nAChR partial agonism may constitute an attractive approach for treating alcohol use disorders exacerbated by elevated stress response.
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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.