ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2014
Conserved single residue in the BK potassium channel required for activation by alcohol and intoxication in C. elegans.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 45 citations in OpenAlex.
- Advances in drug addiction research usingFrontiers in cell and developmental biology · 2026Review
- High-throughput assessment of the behavioral responses to toxic organic solvents in Caenorhabditis elegans.PloS one · 2025Article
- Ethanol alters mechanosensory habituation in C. elegans by way of the BK potassium channel through a novel mechanism.PloS one · 2025Article
- Hispidol Regulates Behavioral Responses to Ethanol through Modulation of BK Channels: A Novel Candidate for the Treatment of Alcohol Use Disorder.Molecules (Basel, Switzerland) · 2024Article
- Natural variation in protein kinase D modifies alcohol sensitivity inbioRxiv : the preprint server for biology · 2024Article
- Ethanol's interaction with BK channel α subunit residue K361 does not mediate behavioral responses to alcohol in mice.Molecular psychiatry · 2024Article
- Large conductance voltage-and calcium-activated KFrontiers in pharmacology · 2024Review
- Transgenerational effects of alcohol on behavioral sensitivity to alcohol in Caenorhabditis elegans.PloS one · 2022Article
- Electrophysiological Properties of Ion Channels in Ascaris suum Tissue Incorporated into Planar Lipid Bilayers.The Korean journal of parasitology · 2021Article
- Transcriptional analysis of the response of C. elegans to ethanol exposure.Scientific reports · 2021Article
- BK channel clustering is required for normal behavioral alcohol sensitivity in C. elegans.Scientific reports · 2019Article
- Caenorhabditis elegans as a model system to identify therapeutics for alcohol use disorders.Behavioural brain research · 2019Article
- A Novel Peptide Restricts Ethanol Modulation of the BK Channel In Vitro and In Vivo.The Journal of pharmacology and experimental therapeutics · 2018Article
- GCY-35/GCY-36-TAX-2/TAX-4 Signalling in OScientific reports · 2018Article
- SLO potassium channels antagonize premature decision making inCommunications biology · 2018Article
- Article
- Behavioral Deficits Following Withdrawal from Chronic Ethanol Are Influenced by SLO Channel Function inGenetics · 2017Article
- Titrating Tipsy Targets: The Neurobiology of Low-Dose Alcohol.Trends in pharmacological sciences · 2017Review
- ERG-28 controls BK channel trafficking in the ER to regulate synaptic function and alcohol response ineLife · 2017Article
- The residue I257 at S4-S5 linker in KCNQ1 determines KCNQ1/KCNE1 channel sensitivity to 1-alkanols.Acta pharmacologica Sinica · 2016Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Alcohol directly modulates the BK potassium channel to alter behaviors in species ranging from invertebrates to humans. In the nematode Caenorhabditis elegans, mutations that eliminate the BK channel, SLO-1, convey dramatic resistance to intoxication by ethanol. We hypothesized that certain conserved amino acids are critical for ethanol modulation, but not for basal channel function. To identify such residues, we screened C. elegans strains with different missense mutations in the SLO-1 channel. A strain with the SLO-1 missense mutation T381I in the RCK1 domain was highly resistant to intoxication. This mutation did not interfere with other BK channel-dependent behaviors, suggesting that the mutant channel retained normal in vivo function. Knock-in of wild-type versions of the worm or human BK channel rescued intoxication and other BK channel-dependent behaviors in a slo-1-null mutant background. In contrast, knock-in of the worm T381I or equivalent human T352I mutant BK channel selectively rescued BK channel-dependent behaviors while conveying resistance to intoxication. Single-channel patch-clamp recordings confirmed that the human BK channel engineered with the T352I missense mutation was insensitive to activation by ethanol, but otherwise had normal conductance, potassium selectivity, and only subtle differences in voltage dependence. Together, our behavioral and electrophysiological results demonstrate that the T352I mutation selectively disrupts ethanol modulation of the BK channel. The T352I mutation may alter a binding site for ethanol and/or interfere with ethanol-induced conformational changes that are critical for behavioral responses to ethanol.
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