ArticleJournal of neuroscience research2009
Overexpression of glycogen synthase kinase 3beta sensitizes neuronal cells to ethanol toxicity.
Article in Journal of neuroscience research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 56 citations in OpenAlex.
- Postnatal Day 7 Ethanol Exposure is Associated with Apoptosis-Related Changes in GAD67-Positive Neurons and Candidate CaMKII/GSK-3β/BAX Signaling in the Mouse Spinal Dorsal Horn.Substance abuse and rehabilitation · 2026Article
- Mechanisms of Alcohol Interference with Hippocampal Neurogenesis and its Repair Strategies.Molecular neurobiology · 2025Review
- Ethanol sustains phosphorylated tau protein in the cultured neonatal rat hippocampus: Implications for fetal alcohol spectrum disorders.Alcohol (Fayetteville, N.Y.) · 2022Article
- Standardization ofFrontiers in pharmacology · 2021Article
- Alcohol-Induced Neuroinflammatory Response and Mitochondrial Dysfunction on Aging and Alzheimer's Disease.Frontiers in behavioral neuroscience · 2021Review
- Alcohol Use Disorder, Neurodegeneration, Alzheimer's and Parkinson's Disease: Interplay Between Oxidative Stress, Neuroimmune Response and Excitotoxicity.Frontiers in cellular neuroscience · 2020Review
- Ethanol Impairs NRF2/Antioxidant and Growth Signaling in the Intact Placenta In Vivo and in Human Trophoblasts.Biomolecules · 2019Article
- Minocycline attenuates ethanol-induced cell death and microglial activation in the developing spinal cord.Alcohol (Fayetteville, N.Y.) · 2019Article
- Function and Mechanism of Myelin Regulation in Alcohol Abuse and Alcoholism.BioEssays : news and reviews in molecular, cellular and developmental biology · 2019Review
- Role of MCP-1 and CCR2 in alcohol neurotoxicity.Pharmacological research · 2019Review
- 4-Phenylbutyric Acid Protects Against Ethanol-Induced Damage in the Developing Mouse Brain.Alcoholism, clinical and experimental research · 2019Article
- Role of MCP-1 and CCR2 in ethanol-induced neuroinflammation and neurodegeneration in the developing brain.Journal of neuroinflammation · 2018Article
- Binge Alcohol Exposure Causes Neurobehavioral Deficits and GSK3β Activation in the Hippocampus of Adolescent Rats.Scientific reports · 2018Article
- Ethanol stimulates the in vivo axonal movement of neuropeptide dense-core vesicles in Drosophila motor neurons.Journal of neurochemistry · 2018Article
- Minocycline protects developing brain against ethanol-induced damage.Neuropharmacology · 2018Article
- Effects of chronic alcohol exposure on ischemia-reperfusion-induced acute kidney injury in mice: the role of β-arrestin 2 and glycogen synthase kinase 3.Experimental & molecular medicine · 2017Article
- Effects of selection for ethanol preference on gene expression in the nucleus accumbens of HS-CC mice.Genes, brain, and behavior · 2017Article
- Neuronal survival in the brain: neuron type-specific mechanisms.Cell death & disease · 2017Review
- Acute Ethanol Inhibition of γ Oscillations Is Mediated by Akt and GSK3β.Frontiers in cellular neuroscience · 2016Article
- Ethanol Activation of PKA Mediates Single-Minded 2 Expression in Neuronal Cells.Molecular neurobiology · 2015Article
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 2 countries.
Funding
Abstract
The developing central nervous system (CNS) is particularly susceptible to ethanol toxicity. The loss of neurons underlies many of the behavioral deficits observed in fetal alcohol spectrum disorders (FASD). The mechanisms of ethanol-induced neuronal loss, however, remain incompletely elucidated. We demonstrated that glycogen synthase kinase 3beta (GSK3beta), a multifunctional serine/threonine kinase, was involved in ethanol neurotoxicity. The activity of GSK3beta is negatively regulated by its phosphorylation at serine 9 (Ser9). Ethanol induced dephosphorylation of GSK3beta at Ser9 and the activation of Bax as well as caspase-3 in the developing mouse brain. These ethanol-induced alterations were ameliorated by the pretreatment of a GSK3beta inhibitor, lithium. To determine the role of GSK3beta in ethanol neurotoxicity, we overexpressed wild-type (WT), S9A mutant or dominant-negative (DN) mutant GSK3beta in a neuronal cell line (SK-N-MC). Ethanol only modestly reduced the viability of parental SK-N-MC cells but drastically induced caspase-3 activation and apoptosis in cells overexpressing WT or S9A GSK3beta, indicating that the high levels of GSK3beta or the active form of GSK3beta increased cellular sensitivity to ethanol. Contrarily, overexpression of DN GSK3beta conferred resistance to ethanol toxicity. Lithium and other specific GSK3beta inhibitors abolished the hypersensitivity to ethanol caused by WT or S9A overexpression. Bax, a proapoptotic protein, is a substrate of GSK3beta. Cells overexpressing WT or S9A GSK3beta were much more sensitive to ethanol-induced Bax activation than parental SK-N-MC cells. Our results indicate that GSK3beta may be a mediator of ethanol neurotoxicity, and its expression status in a cell may determine ethanol vulnerability.
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