ArticleBritish journal of pharmacology2014
The α3β4* nicotinic ACh receptor subtype mediates physical dependence to morphine: mouse and human studies.
Article in British journal of pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 38 citations in OpenAlex.
- Characterization and validation of a spontaneous acute and protracted oxycodone withdrawal model in male and female mice.Pharmacology, biochemistry, and behavior · 2024Article
- New medications development for smoking cessation.Addiction neuroscience · 2023Article
- What We Have Gained from Ibogaine: α3β4 Nicotinic Acetylcholine Receptor Inhibitors as Treatments for Substance Use Disorders.Journal of medicinal chemistry · 2023Review
- Review
- Linking the CHRNA5 SNP to drug abuse liability: From circuitry to cellular mechanisms.Neuropharmacology · 2021Review
- α3* Nicotinic Acetylcholine Receptors in the Habenula-Interpeduncular Nucleus Circuit Regulate Nicotine Intake.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Neuronal nicotinic acetylcholine receptors mediate ∆Addiction biology · 2020Article
- Early adolescent nicotine exposure affects later-life hippocampal mu-opioid receptors activity and morphine reward but not physical dependence in male mice.Pharmacology, biochemistry, and behavior · 2018Article
- α-Conotoxins active at α3-containing nicotinic acetylcholine receptors and their molecular determinants for selective inhibition.British journal of pharmacology · 2018Review
- Design, synthesis, and biological activity of 5'-phenyl-1,2,5,6-tetrahydro-3,3'-bipyridine analogues as potential antagonists of nicotinic acetylcholine receptors.Bioorganic & medicinal chemistry letters · 2017Article
- α-Conotoxin [S9A]TxID Potently Discriminates between α3β4 and α6/α3β4 Nicotinic Acetylcholine Receptors.Journal of medicinal chemistry · 2017Article
- Oxycodone physical dependence and its oral self-administration in C57BL/6J mice.European journal of pharmacology · 2016Article
- Enhanced Sensitivity of α3β4 Nicotinic Receptors in Enteric Neurons after Long-Term Morphine: Implication for Opioid-Induced Constipation.The Journal of pharmacology and experimental therapeutics · 2016Article
- African-specific variability in the acetylcholine muscarinic receptor M4: association with cocaine and heroin addiction.Pharmacogenomics · 2016Article
- Nicotinic acetylcholine receptors: upregulation, age-related effects and associations with drug use.Genes, brain, and behavior · 2016Review
- UBXN2A regulates nicotinic receptor degradation by modulating the E3 ligase activity of CHIP.Biochemical pharmacology · 2015Article
- AT-1001 Is a Partial Agonist with High Affinity and Selectivity at Human and Rat α3β4 Nicotinic Cholinergic Receptors.Molecular pharmacology · 2015Article
- Nicotinic Mechanisms Modulate Ethanol Withdrawal and Modify Time Course and Symptoms Severity of Simultaneous Withdrawal from Alcohol and Nicotine.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2015Article
- Pharmacological stress is required for the anti-alcohol effect of the α3β4* nAChR partial agonist AT-1001.Neuropharmacology · 2015Article
- Assessment of affective and somatic signs of ethanol withdrawal in C57BL/6J mice using a short-term ethanol treatment.Alcohol (Fayetteville, N.Y.) · 2015Article
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Authors and funding
16 authors at 7 institutions in 3 countries.
Funding
Abstract
background and purposeRecent data have indicated that α3β4* neuronal nicotinic (n) ACh receptors may play a role in morphine dependence. Here we investigated if nACh receptors modulate morphine physical withdrawal. EXPERIMENTAL APPROACHES: To assess the role of α3β4* nACh receptors in morphine withdrawal, we used a genetic correlation approach using publically available datasets within the GeneNetwork web resource, genetic knockout and pharmacological tools. Male and female European-American (n = 2772) and African-American (n = 1309) subjects from the Study of Addiction: Genetics and Environment dataset were assessed for possible associations of polymorphisms in the 15q25 gene cluster and opioid dependence. KEY
resultsBXD recombinant mouse lines demonstrated an increased expression of α3, β4 and α5 nACh receptor mRNA in the forebrain and midbrain, which significantly correlated with increased defecation in mice undergoing morphine withdrawal. Mice overexpressing the gene cluster CHRNA5/A3/B4 exhibited increased somatic signs of withdrawal. Furthermore, α5 and β4 nACh receptor knockout mice expressed decreased somatic withdrawal signs compared with their wild-type counterparts. Moreover, selective α3β4* nACh receptor antagonists, α-conotoxin AuIB and AT-1001, attenuated somatic signs of morphine withdrawal in a dose-related manner. In addition, two human datasets revealed a protective role for variants in the CHRNA3 gene, which codes for the α3 nACh receptor subunit, in opioid dependence and withdrawal. In contrast, we found that the α4β2* nACh receptor subtype is not involved in morphine somatic withdrawal signs. CONCLUSION AND IMPLICATIONS: Overall, our findings suggest an important role for the α3β4* nACh receptor subtype in morphine physical dependence.
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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.