ArticleAlcoholism, clinical and experimental research2015
BK Channel β1 Subunit Contributes to Behavioral Adaptations Elicited by Chronic Intermittent Ethanol Exposure.
Article in Alcoholism, clinical and experimental research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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.
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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
9 citing papers in PubMed, 13 citations in OpenAlex.
- Ethanol's interaction with BK channel α subunit residue K361 does not mediate behavioral responses to alcohol in mice.Molecular psychiatry · 2024Article
- Does tolerance to ethanol-induced ataxia explain the sensitized response to ethanol?Frontiers in psychiatry · 2024Article
- KCurrent neuropharmacology · 2023Review
- Leveraging Neural Networks in Preclinical Alcohol Research.Brain sciences · 2020Review
- Genetic studies of alcohol dependence in the context of the addiction cycle.Neuropharmacology · 2017Review
- Modulation of BK Channel Function by Auxiliary Beta and Gamma Subunits.International review of neurobiology · 2016Review
- BK Channels in the Central Nervous System.International review of neurobiology · 2016Review
- Modulation of BK Channels by Ethanol.International review of neurobiology · 2016Review
- BK channels and alcohol tolerance: Insights from studies onMedicine internationalArticle
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
backgroundLarge conductance, calcium- and voltage-activated potassium (BK) channels regulate neuronal excitability and neurotransmission. They can be directly activated by ethanol (EtOH) and they may be implicated in EtOH dependence. In this study, we sought to determine the influence of the auxiliary β1 and β4 subunits on EtOH metabolism, acute sensitivity to EtOH intoxication, acute functional tolerance, chronic tolerance, and handling-induced convulsions during withdrawal.
methodsMotor coordination, righting reflex, and body temperature were evaluated in BK β1 and β4 knockout, heterozygous, and wild-type mice following acute EtOH administration. Chronic tolerance and physical dependence were induced by chronic intermittent inhalation of EtOH vapor.
resultsConstitutive deficiency in BK β1 or β4 subunits did not alter the clearance rate of EtOH, acute sensitivity to EtOH-induced ataxia, sedation, and hypothermia, nor acute functional tolerance to ataxia. BK β1 deletion reduced chronic tolerance to sedation and abolished chronic tolerance to hypothermia, while BK β4 deletion did not affect these adaptations to chronic EtOH exposure. Finally, the absence of BK β1 accelerated the appearance, while the absence of BK β4 delayed the resolution, of the hyperexcitable state associated with EtOH withdrawal.
conclusionsAltogether, the present findings reveal the critical role of BK β1 in behavioral adaptations to prolonged, repeated EtOH intoxication.
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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.