ArticleJournal of neuroscience research2021
Ethanol modulation of cerebellar neuroinflammation in a postnatal mouse model of fetal alcohol spectrum disorders.
Article in Journal of neuroscience research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
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Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 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
- Neurosteroid (3α,5α)3-hydroxypregnan-20-one enhancement of anti-inflammatory chemokine CX3CL1 exhibits sex, brain region, and cellular specificity in alcohol-preferring rats.Psychopharmacology · 2026Article
- Molecular Networks of Redox Dysregulation in Fetal Alcohol Spectrum Disorders: Mechanisms and Therapeutic Prospects.Antioxidants (Basel, Switzerland) · 2026Review
- Article
- Gut Microbiome, Neuroinflammation, and Fetal Alcohol Spectrum Disorders: Insights from Rodent Models.Biology · 2025Review
- Identification of the microglia-associated signature in experimental autoimmune encephalomyelitis.Frontiers in immunology · 2025Article
- Ethanol modulates astrocyte activation and neuroinflammation via miR-339/NLRP6 inflammasome signaling.Free radical biology & medicine · 2025Article
- Impact of Intrauterine Insults on Fetal and Postnatal Cerebellar Development in Humans and Rodents.Cells · 2024Review
- Alcohol Toxicity in the Developing Cerebellum.Diagnostics (Basel, Switzerland) · 2024Article
- An overview of current advances in perinatal alcohol exposure and pathogenesis of fetal alcohol spectrum disorders.Journal of neurodevelopmental disorders · 2024Review
- Developmental Ethanol Exposure Impacts Purkinje Cells but Not Microglia in the Young Adult Cerebellum.Cells · 2024Article
- Article
- Impact of miR-29c-3p in the Nucleus Accumbens on Methamphetamine-Induced Behavioral Sensitization and Neuroplasticity-Related Proteins.International journal of molecular sciences · 2024Article
- GPR37 and its neuroprotective mechanisms: bridging osteocalcin signaling and brain function.Frontiers in cell and developmental biology · 2024Review
- The interaction of genetic sex and prenatal alcohol exposure on health across the lifespan.Frontiers in neuroendocrinology · 2023Review
- Orphan G Protein-Coupled Receptor GPR37 as an Emerging Therapeutic Target.ACS chemical neuroscience · 2023Review
- Effects of chronic and binge ethanol administration on mouse cerebellar and hippocampal neuroinflammation.The American journal of drug and alcohol abuse · 2023Article
- Article
- Ethanol-induced cerebellar transcriptomic changes in a postnatal model of fetal alcohol spectrum disorders: Focus on disease onset.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
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Fetal alcohol spectrum disorders (FASD) are alarmingly common, result in significant personal and societal loss, and there is no effective treatment for these disorders. Cerebellar neuropathology is common in FASD and causes aberrant cognitive and motor function. Ethanol-induced neuroinflammation is believed to contribute to neuropathological sequelae of FASD, and was previously demonstrated in the cerebellum in animal models of FASD. We now demonstrate neuroinflammation persists in the cerebellum several days following cessation of ethanol treatment in an early postnatal mouse model, with meaningful implications for timing of therapeutic intervention in FASD. We also demonstrate by Sholl analysis that ethanol decreases ramification of microglia cell processes in cells located near the Purkinje cell layer but not those near the external granule cell layer. Ethanol did not alter the expression of anti-inflammatory molecules or molecules that constitute NLRP1 and NLRP3 inflammasomes. Interestingly, ethanol decreased the expression of IL-23a (P19) and IL-12Rβ1 suggesting that ethanol may suppress IL-12 and IL-23 signaling. Fractalkine-fractalkine receptor (CX3CL1-CX3CR1) signaling is believed to suppress microglial activation and our demonstration that ethanol decreases CX3CL1 expression suggests that ethanol modulation of CX3CL1-CX3CR1 signaling may contribute to cerebellar neuroinflammation and neuropathology. We demonstrate ethanol alters the expression of specific molecules in the cerebellum understudied in FASD, but crucial for immune responses. Ethanol increases the expression of NOX-2 and NGP and decreases the expression of RAG1, NOS1, CD59a, S1PR5, PTPN22, GPR37, and Serpinb1b. These molecules represent a new horizon as potential targets for development of FASD therapy.
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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.