Evidence map›Paper›PMID 27238266›Full record

ReviewInternational review of neurobiology2016

Modulation of BK Channels by Ethanol.

A M Dopico, A N Bukiya, G Kuntamallappanavar, J Liu

Abstract readReview
In one paragraph

Review in International review of neurobiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
5.4field-weighted citation impact, top 4% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

24 citing papers in PubMed, 35 citations in OpenAlex.

  1. Potential therapeutic targeting of BKMolecular oncology · 2026
    Review
  2. Review
  3. Review
  4. Toluene Toxicity in the Brain: From Cellular Targets to Molecular Mechanisms.Annual review of pharmacology and toxicology · 2025
    Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. BK Channel Regulation of Afterpotentials and Burst Firing in Cerebellar Purkinje Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. A Novel Peptide Restricts Ethanol Modulation of the BK Channel In Vitro and In Vivo.The Journal of pharmacology and experimental therapeutics · 2018
    Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

A M DopicoCollege of Medicine, The University of Tennessee Health Science Center, Memphis, TN, United States. Electronic address: adopico@uthsc.edu.
A N BukiyaCollege of Medicine, The University of Tennessee Health Science Center, Memphis, TN, United States.
G KuntamallappanavarCollege of Medicine, The University of Tennessee Health Science Center, Memphis, TN, United States.
J LiuCollege of Medicine, The University of Tennessee Health Science Center, Memphis, TN, United States.
University of Tennessee Health Science Center · US

Funding

ETHANOL ACTIONS ON SLO CHANNELS FROM ARTERIES VS BRAINR01AA011560 · NIAAA · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI Alex Dopico · 2001 to 2026
$4.4M
Ethanol actions on slo channels from arteries vs. brainR37AA011560 · NIAAA · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI DOPICO, ALEX M. · 2009 to 2018
$3.6M
Cholesterol control of alcohol-induced cerebral artery constrictionR01AA023764 · NIAAA · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI BUKIYA, ANNA · 2015 to 2019
$1.7M
NIAAA NIH HHS R01 AA011560NIAAA NIH HHS R01 AA023764NIAAA NIH HHS R37 AA011560
6 · The paper itself

Abstract

In alcohol-naïve systems, ethanol (<100mM) exposure of calcium-gated BK channels perturbs physiology and behavior. Brief (several minutes) ethanol exposure usually leads to increased BK current, which results from ethanol interaction with a pocket mapped to the BK channel-forming slo1 protein cytosolic tail domain. The importance of this region in ethanol-induced intoxication has been independently supported by an unbiased screen of Caenorhabditis elegans slo1 mutants. However, ethanol-induced BK activation is not universal as refractoriness and inhibition have been reported. The final effect depends on many factors, including intracellular calcium levels, slo1 isoform, BK beta subunit composition, posttranslational modification of BK proteins, channel lipid microenvironment, and type of ethanol administration. Studies in Drosophila melanogaster, C. elegans, and rodents show that protracted/repeated ethanol administration leads to tolerance to ethanol-induced modification of BK-driven physiology and behavior. Unveiling the mechanisms underlying tolerance is of major importance, as tolerance to ethanol has been proposed as predictor of risk for alcoholism.

Indexed as

AnimalsCentral Nervous System DepressantsEthanolHumansIon Channel GatingLarge-Conductance Calcium-Activated Potassium ChannelsModels, MolecularCentral Nervous System DepressantsEthanolLarge-Conductance Calcium-Activated Potassium ChannelsAlcohol receptorAlcohol tolerance and dependenceBK beta subunitsCaenorhabditis elegansDrosophila melanogasterEthanolEthanol intoxicationIon channel–lipid interactionsRodent models of alcohol-driven behaviorSlo1 protein

Identifiers

PMID27238266
PMCPMC5257281
OpenAlexW2478278060

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.