ArticleExperimental neurology2014
Pre-administration of G9a/GLP inhibitor during synaptogenesis prevents postnatal ethanol-induced LTP deficits and neurobehavioral abnormalities in adult mice.
Article in Experimental neurology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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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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Who cites it
36 citing papers in PubMed, 47 citations in OpenAlex.
- Trial
- The dual G9a inhibitor and histamine H3 receptor antagonist A-366 improves repetitive and social behaviors and attenuates neuroinflammation in BTBR T + tf/J mice.Scientific reports · 2026Article
- Beyond Genes: Mechanistic and Epidemiological Insights into Paternal Environmental Influence on Offspring Health.Current environmental health reports · 2025Review
- Nonconceptus Mechanisms of Prenatal Alcohol Exposure That Disrupt Embryo-Fetal Development: An Integrative View.Alcohol research : current reviews · 2025Review
- Repurposing of Raltitrexed as an Effective G9a/EHMT2 Inhibitor and Promising Anti-Alzheimer's Agent.ACS medicinal chemistry letters · 2023Article
- Review
- Effects of genetics and sex on adolescent behaviors following neonatal ethanol exposure in BXD recombinant inbred strains.Frontiers in neuroscience · 2023Article
- Caspase-3 Inhibition toward Perinatal Protection of the Developing Brain from Environmental Stress.Developmental neuroscience · 2023Review
- Ethanol sustains phosphorylated tau protein in the cultured neonatal rat hippocampus: Implications for fetal alcohol spectrum disorders.Alcohol (Fayetteville, N.Y.) · 2022Article
- Binge-like Prenatal Ethanol Exposure Causes Impaired Cellular Differentiation in the Embryonic Forebrain and Synaptic and Behavioral Defects in Adult Mice.Brain sciences · 2022Article
- In the pursuit of new social neurons. Neurogenesis and social behavior in mice: A systematic review.Frontiers in cell and developmental biology · 2022Review
- Programmed suppression of oxidative phosphorylation and mitochondrial function by gestational alcohol exposure correlate with widespread increases in H3K9me2 that do not suppress transcription.Epigenetics & chromatin · 2021Article
- Histone Methylation Regulation in Neurodegenerative Disorders.International journal of molecular sciences · 2021Review
- Oxidative stress-induced aberrant G9a activation disturbs RE-1-containing neuron-specific genes expression, leading to degeneration in human SH-SY5Y neuroblastoma cells.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2021Article
- Postnatal Ethanol Exposure Activates HDAC-Mediated Histone Deacetylation, Impairs Synaptic Plasticity Gene Expression and Behavior in Mice.The international journal of neuropsychopharmacology · 2020Article
- Postnatal Ethanol-Induced Neurodegeneration Involves CB1R-Mediated β-Catenin Degradation in Neonatal Mice.Brain sciences · 2020Article
- Distinct functions of endogenous cannabinoid system in alcohol abuse disorders.British journal of pharmacology · 2019Review
- CB1R regulates CDK5 signaling and epigenetically controls Rac1 expression contributing to neurobehavioral abnormalities in mice postnatally exposed to ethanol.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2019Article
- Activity-dependent Signaling and Epigenetic Abnormalities in Mice Exposed to Postnatal Ethanol.Neuroscience · 2018Article
- Mechanisms Underlying the Regulation of HP1γ by the NGF-PKA Signaling Pathway.Scientific reports · 2018Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
It has been widely accepted that deficits in neuronal plasticity underlie the cognitive abnormalities observed in fetal alcohol spectrum disorder (FASD). Exposure of rodents to acute ethanol on postnatal day 7 (P7), which is equivalent to the third trimester of fetal development in human, induces long-term potentiation (LTP) and memory deficits in adult animals. However, the molecular mechanisms underlying these deficits are not well understood. Recently, we found that histone H3 dimethylation (H3K9me2), which is mediated by G9a (lysine dimethyltransferase), is responsible for the neurodegeneration caused by ethanol exposure in P7 mice. In addition, pharmacological inhibition of G9a prior to ethanol treatment at P7 normalized H3K9me2 proteins to basal levels and prevented neurodegeneration in neonatal mice. Here, we tested the hypothesis that pre-administration of G9a/GLP inhibitor (Bix-01294, Bix) in conditions in which ethanol induces neurodegeneration would be neuroprotective against P7 ethanol-induced deficits in LTP, memory and social recognition behavior in adult mice. Ethanol treatment at P7 induces deficits in LTP, memory and social recognition in adult mice and these deficits were prevented by Bix pretreatment at P7. Together, these findings provide physiological and behavioral evidence that the long-term harmful consequences on brain function after ethanol exposure with a third trimester equivalent have an epigenetic origin.
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