ArticleBrain, behavior, and immunity2011
Protection of neurons and microglia against ethanol in a mouse model of fetal alcohol spectrum disorders by peroxisome proliferator-activated receptor-γ agonists.
Article in Brain, behavior, and immunity, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers, 1 of them a synthesis that pooled it.
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.
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.
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Who cites it
78 citing papers in PubMed, 1 synthesis or guideline pooled it, 115 citations in OpenAlex.
- Recent breakthroughs in understanding the cerebellum's role in fetal alcohol spectrum disorder: A systematic review.Alcohol (Fayetteville, N.Y.) · 2024Pooled it
- The NKCC1 Antagonist Bumetanide, Administered After Prenatal Alcohol Exposure, Mitigates Ethanol-Induced Aberrance in Tangential Migration of GABAergic Interneurons in Mouse Medial Prefrontal Cortex.Alcohol, clinical & experimental research · 2026Article
- Prenatal Alcohol Exposure: Impact on Neuroimmune Function in the Stress Response and Pain.Advances in experimental medicine and biology · 2026Review
- Animal Models of Prenatal Alcohol Exposure.Advances in experimental medicine and biology · 2026Review
- Ontogenetic Neuroimmune Changes Following Prenatal Alcohol Exposure: Implications for Neurobehavioral Function.Advances in experimental medicine and biology · 2025Review
- Impact of Intrauterine Insults on Fetal and Postnatal Cerebellar Development in Humans and Rodents.Cells · 2024Review
- The Fetal Alcohol Spectrum Disorders-An Overview of Experimental Models, Therapeutic Strategies, and Future Research Directions.Children (Basel, Switzerland) · 2024Review
- Developmental Ethanol Exposure Impacts Purkinje Cells but Not Microglia in the Young Adult Cerebellum.Cells · 2024Article
- Morphology and Fractal-Based Classifications of Neurons and Microglia in Two and Three Dimensions.Advances in neurobiology · 2024Review
- Review
- Effects of chronic and binge ethanol administration on mouse cerebellar and hippocampal neuroinflammation.The American journal of drug and alcohol abuse · 2023Article
- Ethanol-induced cerebellar transcriptomic changes in a postnatal model of fetal alcohol spectrum disorders: Focus on disease onset.Frontiers in neuroscience · 2023Article
- Editorial: Perspectives and recent advances in Fetal Alcohol Spectrum Disorders research.Frontiers in neuroscience · 2023Article
- Developmental ethanol exposure has minimal impact on cerebellar microglial dynamics, morphology, and interactions with Purkinje cells during adolescence.Frontiers in neuroscience · 2023Article
- Proceedings of the 2021 annual meeting of the Fetal Alcohol Spectrum Disorders Study Group.Alcohol (Fayetteville, N.Y.) · 2022Article
- Repetitive binge-like consumption based on the Drinking-in-the-Dark model alters the microglial population in the mouse hippocampus.Journal of integrative neuroscience · 2021Article
- Developmental Stressors Induce Innate Immune Memory in Microglia and Contribute to Disease Risk.International journal of molecular sciences · 2021Review
- Prenatal alcohol-induced sex differences in immune, metabolic and neurobehavioral outcomes in adult rats.Brain, behavior, and immunity · 2021Article
- Ethanol effects on cerebellar myelination in a postnatal mouse model of fetal alcohol spectrum disorders.Alcohol (Fayetteville, N.Y.) · 2021Article
- Sudden cessation of fluoxetine before alcohol drinking reinstatement alters microglial morphology and TLR4/inflammatory neuroadaptation in the rat brain.Brain structure & function · 2021Article
18 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Fetal alcohol spectrum disorders (FASD) result from ethanol exposure to the developing fetus and are the most common cause of mental retardation in the United States. These disorders are characterized by a variety of neurodevelopmental and neurodegenerative anomalies which result in significant lifetime disabilities. Thus, novel therapies are required to limit the devastating consequences of FASD. Neuropathology associated with FASD can occur throughout the central nervous system (CNS), but is particularly well characterized in the developing cerebellum. Rodent models of FASD have previously demonstrated that both Purkinje cells and granule cells, which are the two major types of neurons in the cerebellum, are highly susceptible to the toxic effects of ethanol. The current studies demonstrate that ethanol decreases the viability of cultured cerebellar granule cells and microglial cells. Interestingly, microglia have dual functionality in the CNS. They provide trophic and protective support to neurons. However, they may also become pathologically activated and produce inflammatory molecules toxic to parenchymal cells including neurons. The findings in this study demonstrate that the peroxisome proliferator-activated receptor-γ agonists 15-deoxy-Δ12,15 prostaglandin J2 and pioglitazone protect cultured granule cells and microglia from the toxic effects of ethanol. Furthermore, investigations using a newly developed mouse model of FASD and stereological cell counting methods in the cerebellum elucidate that ethanol administration to neonates is toxic to both Purkinje cell neurons as well as microglia, and that in vivo administration of PPAR-γ agonists protects these cells. In composite, these studies suggest that PPAR-γ agonists may be effective in limiting ethanol-induced toxicity to the developing CNS.
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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.