ArticleGlia2015
Transient activation of microglia following acute alcohol exposure in developing mouse neocortex is primarily driven by BAX-dependent neurodegeneration.
Article in Glia, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
What it found
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Who cites it
54 citing papers in PubMed, 78 citations in OpenAlex.
- From Perinatal Stress to Schizophrenia: The Emerging Role of Glial Pathology.Annals of neurosciences · 2026Review
- High-Dose Ethanol-Induced Immunosuppression Modulates Sex-Specific Disease Outcomes in a Murine Model of Multiple Sclerosis.Biomolecules · 2026Article
- Early abstinence in severe alcohol use disorder: MCP-1 decline, choroid plexus shrinkage, and region-specific grey-matter volume changes.Translational psychiatry · 2026Article
- Microglial activation drives neuronal dysregulation in alcohol-induced seizure susceptibility.Scientific reports · 2025Article
- Synapse Regulation.Advances in neurobiology · 2024Review
- Sensitivity of Hypocretin System to Chronic Alcohol Exposure: A Human and Animal Study.Neuroscience · 2023Article
- Apoptotic cell death in disease-Current understanding of the NCCD 2023.Cell death and differentiation · 2023Review
- Article
- Developmental ethanol exposure has minimal impact on cerebellar microglial dynamics, morphology, and interactions with Purkinje cells during adolescence.Frontiers in neuroscience · 2023Article
- Adolescent ethanol drinking promotes hyperalgesia, neuroinflammation and serotonergic deficits in mice that persist into adulthood.Brain, behavior, and immunity · 2023Article
- The pro-apoptotic Bax gene modifies susceptibility to craniofacial dysmorphology following gastrulation-stage alcohol exposure.Birth defects research · 2022Article
- Choline Supplementation Modifies the Effects of Developmental Alcohol Exposure on Immune Responses in Adult Rats.Nutrients · 2022Article
- Rat Model of Late Gestational Alcohol Exposure Produces Similar Life-Long Changes in Thalamic Nucleus Reuniens Following Moderate- Versus High-Dose Insult.Alcohol and alcoholism (Oxford, Oxfordshire) · 2022Article
- Nonapoptotic caspases in neural development and in anesthesia-induced neurotoxicity.Trends in neurosciences · 2022Review
- 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
- Dynamics of microglia and dendritic spines in early adolescent cortex after developmental alcohol exposure.Developmental neurobiology · 2021Article
- Acute ethanol exposure rapidly alters cerebellar and cortical microglial physiology.The European journal of neuroscience · 2021Article
- Ethanol modulation of cerebellar neuroinflammation in a postnatal mouse model of fetal alcohol spectrum disorders.Journal of neuroscience research · 2021Article
- Neuroinflammatory contribution of microglia and astrocytes in fetal alcohol spectrum disorders.Journal of neuroscience research · 2021Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Fetal alcohol exposure is the most common known cause of preventable mental retardation, yet we know little about how microglia respond to, or are affected by, alcohol in the developing brain in vivo. Using an acute (single day) model of moderate (3 g/kg) to severe (5 g/kg) alcohol exposure in postnatal day (P) 7 or P8 mice, we found that alcohol-induced neuroapoptosis in the neocortex is closely correlated in space and time with the appearance of activated microglia near dead cells. The timing and molecular pattern of microglial activation varied with the level of cell death. Although microglia rapidly mobilized to contact and engulf late-stage apoptotic neurons, apoptotic bodies temporarily accumulated in neocortex, suggesting that in severe cases of alcohol toxicity the neurodegeneration rate exceeds the clearance capacity of endogenous microglia. Nevertheless, most dead cells were cleared and microglia began to deactivate within 1-2 days of the initial insult. Coincident with microglial activation and deactivation, there was a transient increase in expression of pro-inflammatory factors, TNFα and IL-1β, after severe (5 g/kg) but not moderate (3 g/kg) EtOH levels. Alcohol-induced microglial activation and pro-inflammatory factor expression were largely abolished in BAX null mice lacking neuroapoptosis, indicating that microglial activation is primarily triggered by apoptosis rather than the alcohol. Therefore, acute alcohol exposure in the developing neocortex causes transient microglial activation and mobilization, promoting clearance of dead cells and tissue recovery. Moreover, cortical microglia show a remarkable capacity to rapidly deactivate following even severe neurodegenerative insults in the developing brain.
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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.