ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2018
Glycogen synthase kinase 3 beta regulates ethanol consumption and is a risk factor for alcohol dependence.
Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 31 citations in OpenAlex.
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- Differential regulation of G protein-coupled receptor-associated proteins in the caudate and the putamen of cynomolgus macaques following chronic ethanol drinking.Journal of neurochemistry · 2024Article
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- Assessing negative affect in mice during abstinence from alcohol drinking: Limitations and future challenges.Alcohol (Fayetteville, N.Y.) · 2022Review
- Chloride intracellular channel 4 (CLIC4) expression profile in the mouse medial prefrontal cortex and its regulation by ethanol.Alcoholism, clinical and experimental research · 2022Article
- Alcohol and the brain: from genes to circuits.Trends in neurosciences · 2021Review
- Effect of chronic ethanol consumption in rhesus macaques on the nucleus accumbens core transcriptome.Addiction biology · 2021Article
- Mechanisms of Alcohol Addiction: Bridging Human and Animal Studies.Alcohol and alcoholism (Oxford, Oxfordshire) · 2020Review
- Deletion of Glycogen Synthase Kinase-3β in DBiological psychiatry · 2020Article
- Pharmacological inhibition of glycogen synthase kinase 3 increases operant alcohol self-administration in a manner associated with altered pGSK-3β, protein interacting with C kinase and GluA2 protein expression in the reward pathway of male C57BL/6J mice.Behavioural pharmacology · 2020Article
- Systemic Administration of the Cyclin-Dependent Kinase Inhibitor (S)-CR8 Selectively Reduces Escalated Ethanol Intake in Dependent Rats.Alcoholism, clinical and experimental research · 2019Article
- Supraphysiologic-dose anabolic-androgenic steroid use: A risk factor for dementia?Neuroscience and biobehavioral reviews · 2019Review
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- Alcohol drinking exacerbates neural and behavioral pathology in the 3xTg-AD mouse model of Alzheimer's disease.International review of neurobiology · 2019Review
- Article
- GSK3β in the prefrontal cortex: a molecular handle specific to addiction pathology?Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2018Article
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12 authors at 1 institution in 1 country.
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Abstract
Understanding how ethanol actions on brain signal transduction and gene expression lead to excessive consumption and addiction could identify new treatments for alcohol dependence. We previously identified glycogen synthase kinase 3-beta (Gsk3b) as a member of a highly ethanol-responsive gene network in mouse medial prefrontal cortex (mPFC). Gsk3b has been implicated in dendritic function, synaptic plasticity and behavioral responses to other drugs of abuse. Here, we investigate Gsk3b in rodent models of ethanol consumption and as a risk factor for human alcohol dependence. Stereotactic viral vector gene delivery overexpression of Gsk3b in mouse mPFC increased 2-bottle choice ethanol consumption, which was blocked by lithium, a known GSK3B inhibitor. Further, Gsk3b overexpression increased anxiety-like behavior following abstinence from ethanol. Protein or mRNA expression studies following Gsk3b over-expression identified synaptojanin 2, brain-derived neurotrophic factor and the neuropeptide Y Y5 receptor as potential downstream factors altering ethanol behaviors. Rat operant studies showed that selective pharmacologic inhibition of GSK3B with TDZD-8 dose-dependently decreased motivation to self-administer ethanol and sucrose and selectively blocked ethanol relapse-like behavior. In set-based and gene-wise genetic association analysis, a GSK3b-centric gene expression network had significant genetic associations, at a gene and network level, with risk for alcohol dependence in humans. These mutually reinforcing cross-species findings implicate GSK3B in neurobiological mechanisms controlling ethanol consumption, and as both a potential risk factor and therapeutic target for alcohol dependence.
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