ArticleNature communications2020
Gestational alcohol exposure disrupts cognitive function and striatal circuits in adult offspring.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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
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Who cites it
20 citing papers in PubMed, 29 citations in OpenAlex.
- Assessment of GABANeuroscience letters · 2026Article
- Stress disrupts engram ensembles in lateral amygdala to generalize threat memory in mice.Cell · 2025Article
- Transgenerational of Oxidative Damage Induced by Prenatal Ethanol Exposure on Spatial Learning/Memory and BDNF in the of Male Rats.IBRO neuroscience reports · 2024Article
- GABA system as the cause and effect in early development.Neuroscience and biobehavioral reviews · 2024Review
- Sex-specific alterations in cognitive control following moderate prenatal alcohol exposure and transient systemic hypoxia ischemia in the rat.Alcohol, clinical & experimental research · 2024Article
- Impact of low-level prenatal alcohol exposure and maternal stress on autonomic regulation.Pediatric research · 2024Article
- Gestational ethanol exposure impairs motor skills in female mice through dysregulated striatal dopamine and acetylcholine function.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2023Article
- Subpopulations of hypocretin/orexin neurons differ in measures of their cell proliferation, dynorphin co-expression, projections, and response to embryonic ethanol exposure.Scientific reports · 2023Article
- Review
- High-resolution imaging in studies of alcohol effect on prenatal development.Advances in drug and alcohol research · 2023Article
- Postnatal ethanol exposure impairs social behavior and operant extinction in the adult female mouse offspring.Frontiers in neuroscience · 2023Article
- Local modulation by presynaptic receptors controls neuronal communication and behaviour.Nature reviews. Neuroscience · 2022Review
- Chemogenetics as a neuromodulatory approach to treating neuropsychiatric diseases and disorders.Molecular therapy : the journal of the American Society of Gene Therapy · 2022Review
- Alcohol and the brain: from genes to circuits.Trends in neurosciences · 2021Review
- Corticostriatal Circuit Models of Cognitive Impairments Induced by Fetal Exposure to Alcohol.Biological psychiatry · 2021Review
- Enhancement of parvalbumin interneuron-mediated neurotransmission in the retrosplenial cortex of adolescent mice following third trimester-equivalent ethanol exposure.Scientific reports · 2021Article
- Prenatal alcohol exposure reduces posterior dorsomedial striatum excitability and motivation in a sex- and age-dependent fashion.Neuropharmacology · 2020Article
- In utero MRI identifies consequences of early-gestation alcohol drinking on fetal brain development in rhesus macaques.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Article
- Exploring behavioral phenotypes in a mouse model of fetal alcohol spectrum disorders.Developmental neurobiologyArticle
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Fetal alcohol exposure (FAE) is the leading preventable developmental cause of cognitive dysfunction. Even in the absence of binge drinking, alcohol consumption during pregnancy can leave offspring deficient. However, the mechanisms underlying these deficiencies are unknown. Using a mouse model of gestational ethanol exposure (GEE), we show increased instrumental lever-pressing and disruption of efficient habitual actions in adults, indicative of disrupted cognitive function. In vivo electrophysiology reveals disrupted action encoding in dorsolateral striatum (DLS) associated with altered habit learning. GEE mice exhibit decreased GABAergic transmission onto DLS projection neurons, including inputs from parvalbumin interneurons, and increased endocannabinoid tone. Chemogenetic activation of DLS parvalbumin interneurons reduces the elevated lever pressing of GEE mice. Pharmacologically increasing endocannabinoid tone mimics GEE effects on cognition and synaptic transmission. These findings show GEE induces long-lasting deficits in cognitive function that may contribute to human FAE, and identify potential mechanisms for future therapeutic targeting.
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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.