ReviewAlcohol (Fayetteville, N.Y.)2012
K(Ca)2 channels: novel therapeutic targets for treating alcohol withdrawal and escalation of alcohol consumption.
Review in Alcohol (Fayetteville, N.Y.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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
17 citing papers in PubMed.
- DNA Methylation Regulates CDK5R1 and NRBP1 to Exert Effects on Alcohol Dependence: Insights From Mendelian Randomization.Addiction biology · 2026Article
- KAlcohol (Fayetteville, N.Y.) · 2025Article
- Influence of Inherited Seizure Susceptibility on Intermittent Voluntary Alcohol Consumption and Alcohol Withdrawal Seizures in Genetically Epilepsy-Prone Rats (GEPR-3s).Brain sciences · 2024Article
- Research Needs for Inpatient Management of Severe Alcohol Withdrawal Syndrome: An Official American Thoracic Society Research Statement.American journal of respiratory and critical care medicine · 2021Article
- Potassium Channels and Their Potential Roles in Substance Use Disorders.International journal of molecular sciences · 2021Review
- Physiology and Therapeutic Potential of SK, H, and M Medium AfterHyperPolarization Ion Channels.Frontiers in molecular neuroscience · 2021Review
- Flying Together:International journal of molecular sciences · 2020Review
- Differential potassium channel gene regulation in BXD mice reveals novel targets for pharmacogenetic therapies to reduce heavy alcohol drinking.Alcohol (Fayetteville, N.Y.) · 2017Article
- Neurobiology of comorbid post-traumatic stress disorder and alcohol-use disorder.Genes, brain, and behavior · 2017Review
- Effects of chronic alcohol consumption on neuronal function in the non-human primate BNST.Addiction biology · 2016Article
- Increased Basolateral Amygdala Pyramidal Cell Excitability May Contribute to the Anxiogenic Phenotype Induced by Chronic Early-Life Stress.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- KCNN Genes that Encode Small-Conductance Ca2+-Activated K+ Channels Influence Alcohol and Drug Addiction.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2015Article
- Glutathione and redox signaling in substance abuse.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2014Review
- Neurochemical mechanisms of alcohol withdrawal.Handbook of clinical neurology · 2014Review
- Transcriptome analysis of Inbred Long Sleep and Inbred Short Sleep mice.Genes, brain, and behavior · 2013Article
- Novel anticonvulsants for reducing alcohol consumption: A review of evidence from preclinical rodent drinking models.OA alcohol · 2013Article
- Chronic Alcohol, Intrinsic Excitability, and Potassium Channels: Neuroadaptations and Drinking Behavior.Handbook of experimental pharmacologyArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author.
Funding
Abstract
Small-conductance, calcium-activated potassium (K(Ca)2) channels influence neuronal firing properties, intrinsic excitability, and NMDA receptor-dependent synaptic responses and plasticity. In this mini-review, we discuss new evidence that chronic alcohol-associated plasticity critically involves K(Ca)2 channels in hippocampus, ventral tegmental area, and nucleus accumbens. K(Ca)2 channel activity can modulate the magnitude of excitation of midbrain dopamine neurons induced by acute alcohol exposure. Emerging evidence indicates that K(Ca)2 channels regulate neuroadaptations to chronic alcohol that contribute to withdrawal hyperexcitability and escalation of voluntary alcohol consumption. Restoring K(Ca)2 channel activity can attenuate the severity of the alcohol withdrawal syndrome in vivo and withdrawal-associated neurotoxicity in vitro. Pharmacological modulation of K(Ca)2 channels can bi-directionally influence drinking behavior in rat and mouse models of voluntary alcohol consumption. Collectively, these studies using various rodent models have clearly indicated a central role for K(Ca)2 channels in the neuroplasticity of chronic alcohol exposure. In addition, accumulating evidence suggests that K(Ca)2 channels are a novel therapeutic target to alleviate the symptoms of alcohol withdrawal and reduce high amounts of alcohol drinking.
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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.