ReviewFrontiers in physiology2014
Ethanol modulation of mammalian BK channels in excitable tissues: molecular targets and their possible contribution to alcohol-induced altered behavior.
Review in Frontiers in physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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.
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.
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Who cites it
28 citing papers in PubMed, 53 citations in OpenAlex.
- Cholesterol and docosahexaenoic acid likely protect against alcohol-induced constriction of cerebral arteries via a common pathway.Advances in drug and alcohol research · 2026Article
- Ethanol alters mechanosensory habituation in C. elegans by way of the BK potassium channel through a novel mechanism.PloS one · 2025Article
- Toluene Toxicity in the Brain: From Cellular Targets to Molecular Mechanisms.Annual review of pharmacology and toxicology · 2025Review
- Changes in the Properties of Ethanol-Sensitive Molecular Targets During Maturation and Aging.Advances in experimental medicine and biology · 2025Review
- Synaptic Mechanisms of Ethanol Tolerance and Neuroplasticity: Insights from Invertebrate Models.International journal of molecular sciences · 2024Review
- Natural variation in protein kinase D modifies alcohol sensitivity inbioRxiv : the preprint server for biology · 2024Article
- Aging in nucleus accumbens and its impact on alcohol use disorders.Alcohol (Fayetteville, N.Y.) · 2023Review
- Alcohol Use Disorder: Neurobiology and Therapeutics.Biomedicines · 2022Review
- Upregulation of Beta4 subunit of BKMolecular brain · 2020Article
- Nicotine and alcohol: the role of midbrain dopaminergic neurons in drug reinforcement.The European journal of neuroscience · 2019Review
- BK channel clustering is required for normal behavioral alcohol sensitivity in C. elegans.Scientific reports · 2019Article
- A Novel Peptide Restricts Ethanol Modulation of the BK Channel In Vitro and In Vivo.The Journal of pharmacology and experimental therapeutics · 2018Article
- Review
- BK β1 subunit-dependent facilitation of ethanol inhibition of BK current and cerebral artery constriction is mediated by the β1 transmembrane domain 2.British journal of pharmacology · 2017Article
- Alcohol and basal ganglia circuitry: Animal models.Neuropharmacology · 2017Review
- Thirst sensation and oral dryness following alcohol intake.The Japanese dental science review · 2017Review
- Behavioral Deficits Following Withdrawal from Chronic Ethanol Are Influenced by SLO Channel Function inGenetics · 2017Article
- Common structural features of cholesterol binding sites in crystallized soluble proteins.Journal of lipid research · 2017Review
- Ethanol-Sensitive Pacemaker Neurons in the Mouse External Globus Pallidus.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2017Article
- Selective alterations of NMDAR function and plasticity in D1 and D2 medium spiny neurons in the nucleus accumbens shell following chronic intermittent ethanol exposure.Neuropharmacology · 2017Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
In most tissues, the function of Ca(2+)- and voltage-gated K(+) (BK) channels is modified in response to ethanol concentrations reached in human blood during alcohol intoxication. In general, modification of BK current from ethanol-naïve preparations in response to brief ethanol exposure results from changes in channel open probability without modification of unitary conductance or change in BK protein levels in the membrane. Protracted and/or repeated ethanol exposure, however, may evoke changes in BK expression. The final ethanol effect on BK open probability leading to either BK current potentiation or BK current reduction is determined by an orchestration of molecular factors, including levels of activating ligand (Ca(2+) i), BK subunit composition and post-translational modifications, and the channel's lipid microenvironment. These factors seem to allosterically regulate a direct interaction between ethanol and a recognition pocket of discrete dimensions recently mapped to the channel-forming (slo1) subunit. Type of ethanol exposure also plays a role in the final BK response to the drug: in several central nervous system regions (e.g., striatum, primary sensory neurons, and supraoptic nucleus), acute exposure to ethanol reduces neuronal excitability by enhancing BK activity. In contrast, protracted or repetitive ethanol administration may alter BK subunit composition and membrane expression, rendering the BK complex insensitive to further ethanol exposure. In neurohypophyseal axon terminals, ethanol potentiation of BK channel activity leads to a reduction in neuropeptide release. In vascular smooth muscle, however, ethanol inhibition of BK current leads to cell contraction and vascular constriction.
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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.