ArticleNeuropharmacology2019
Alpha6-containing nicotinic acetylcholine receptor is a highly sensitive target of alcohol.
Article in Neuropharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.
- The role of nicotinic receptors in alcohol consumption.Pharmacological research · 2023Pooled it
- Shared mechanisms of dopamine and ATP transmission in the nucleus accumbens.bioRxiv : the preprint server for biology · 2026Article
- Adolescent social isolation associated changes in ethanol-induced dopamine regulation in the ventral pallidum.Addiction neuroscience · 2025Article
- "Unraveling the role ofReceptors (Basel, Switzerland) · 2025Article
- Catharanthine Modulates Mesolimbic Dopamine Transmission and Nicotine Psychomotor Effects via Inhibition of α6-Nicotinic Receptors and Dopamine Transporters.ACS chemical neuroscience · 2024Article
- Ivermectin increases striatal cholinergic activity to facilitate dopamine terminal function.Cell & bioscience · 2024Article
- Role of α6-Nicotinic Receptors in Alcohol-Induced GABAergic Synaptic Transmission and Plasticity to Cholinergic Interneurons in the Nucleus Accumbens.Molecular neurobiology · 2023Article
- Molecular Toxicology and Pathophysiology of Comorbid Alcohol Use Disorder and Post-Traumatic Stress Disorder Associated with Traumatic Brain Injury.International journal of molecular sciences · 2023Review
- Molecular Determinants of Species Specificity of α-Conotoxin TxIB towards Rat and Human α6/α3β4 Nicotinic Acetylcholine Receptors.International journal of molecular sciences · 2023Article
- Role of Cannabinoid CB2 Receptor in Alcohol Use Disorders: From Animal to Human Studies.International journal of molecular sciences · 2022Review
- Effectiveness and Relationship between Biased and Unbiased Measures of Dopamine Release and Clearance.ACS chemical neuroscience · 2022Article
- Regional and sex differences in spontaneous striatal dopamine transmission.Journal of neurochemistry · 2022Article
- Targeting prefrontal cortex GABAergic microcircuits for the treatment of alcohol use disorder.Frontiers in synaptic neuroscience · 2022Review
- Modulation of dopamine release by ethanol is mediated by atypical GABAAddiction biology · 2022Article
- Article
- Ethanol interaction with α3β4 nicotinic acetylcholine receptors in neurons of the laterodorsal tegmentum.Alcoholism, clinical and experimental research · 2021Article
- Modified Snake α-Neurotoxin Averts β-Amyloid Binding to α7 Nicotinic Acetylcholine Receptor and Reverses Cognitive Deficits in Alzheimer's Disease Mice.Molecular neurobiology · 2021Article
- An acetylcholine-dopamine interaction in the nucleus accumbens and its involvement in ethanol's dopamine-releasing effect.Addiction biology · 2021Article
- The role of nicotinic acetylcholine receptors in alcohol-related behaviors.Brain research bulletin · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 3 institutions in 2 countries.
Funding
Abstract
Alcohol use disorder (AUD) is a serious public health problem that results in tremendous social, legal and medical costs to society. Unlike other addictive drugs, there is no specific molecular target for ethanol (EtOH). Here, we report a novel molecular target that mediates EtOH effects at concentrations below those that cause legally-defined inebriation. Using patch-clamp recording of human α6*-nicotinic acetylcholine receptor (α6*-nAChR) function when heterologously expressed in SH-EP1 human epithelial cells, we found that 0.1-5 mM EtOH significantly enhances α6*-nAChR-mediated currents with effects that are dependent on both EtOH and nicotine concentrations. EtOH exposure increased both whole-cell current rising slope and decay constants. This EtOH modulation was selective for α6*-nAChRs since it did not affect α3β4-, α4β2-, or α7-nAChRs. In addition, 5 mM EtOH also increased the frequency and amplitude of dopaminergic neuron transients in mouse brain nucleus accumbens slices, that were blocked by the α6*-nAChR antagonist, α-conotoxin MII, suggesting a role for native α6*-nAChRs in low-dose EtOH effects. Collectively, our data suggest that α6*-nAChRs are sensitive targets mediating low-dose EtOH effects through a positive allosteric mechanism, which provides new insight into mechanisms involved in pharmacologically-relevant alcohol effects contributing to AUD.
Indexed as
Identifiers
What OpenQuestion holds
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.