ArticlePloS one2014
Prenatal alcohol exposure modifies glucocorticoid receptor subcellular distribution in the medial prefrontal cortex and impairs frontal cortex-dependent learning.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 48 citations in OpenAlex.
- A Single Dose of a Psychedelic Drug Repairs Prefrontal Cortex Synaptic Physiology in a Mouse Model of Prenatal Alcohol Exposure.Brain and behavior · 2026Article
- Abnormal Magnetic Resonance Imaging in the Medial Prefrontal Cortex following Prenatal Alcohol Exposure and Placental Insufficiency in a Preclinical Model.Developmental neuroscience · 2025Article
- Recent Advances in the Role of Non-coding RNAs in Fetal Alcohol Spectrum Disorders.Advances in experimental medicine and biology · 2025Review
- Independent and Combined Effects of Prenatal Alcohol Exposure and Prenatal Stress on Fetal HPA Axis Development.International journal of molecular sciences · 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
- Postnatal ethanol exposure impairs social behavior and operant extinction in the adult female mouse offspring.Frontiers in neuroscience · 2023Article
- Corticostriatal Circuit Models of Cognitive Impairments Induced by Fetal Exposure to Alcohol.Biological psychiatry · 2021Review
- Chronic alcohol exposure during critical developmental periods differentially impacts persistence of deficits in cognitive flexibility and related circuitry.International review of neurobiology · 2021Review
- Moderate prenatal alcohol exposure impairs cognitive control, but not attention, on a rodent touchscreen continuous performance task.Genes, brain, and behavior · 2021Article
- Moderate Prenatal Alcohol Exposure Impairs Visual-Spatial Discrimination in a Sex-Specific Manner: Effects of Testing Order and Difficulty on Learning Performance.Alcoholism, clinical and experimental research · 2020Article
- Prenatal Alcohol Exposure Results in Sex-Specific Alterations in Circular RNA Expression in the Developing Mouse Brain.Frontiers in neuroscience · 2020Article
- Glucocorticoid receptor expression in the stress-limbic circuitry is differentially affected by prenatal alcohol exposure and adolescent stress.Brain research · 2019Article
- Increased Maternal Care Rescues Altered Reinstatement Responding Following Moderate Prenatal Alcohol Exposure.Alcoholism, clinical and experimental research · 2019Article
- Interactive effects of prenatal alcohol exposure and chronic stress in adulthood on anxiety-like behavior and central stress-related receptor mRNA expression: Sex- and time-dependent effects.Psychoneuroendocrinology · 2018Article
- Prenatal Ethanol Exposure and Neocortical Development: A Transgenerational Model of FASD.Cerebral cortex (New York, N.Y. : 1991) · 2018Article
- Effects of prenatal alcohol exposure (PAE): insights into FASD using mouse models of PAE.Biochemistry and cell biology = Biochimie et biologie cellulaire · 2018Review
- Reversal learning and experimenter-administered chronic intermittent ethanol exposure in male rats.Psychopharmacology · 2016Article
- Changes in the glucocorticoid receptor and Ca²⁺/calreticulin-dependent signalling pathway in the medial prefrontal cortex of rats with post-traumatic stress disorder.Journal of molecular neuroscience : MN · 2015Article
- The impact of prenatal alcohol exposure on hippocampal-dependent outcome measures is influenced by prenatal and early-life rearing conditions.Alcoholism, clinical and experimental research · 2015Article
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Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Prenatal alcohol exposure (PAE) has been shown to impair learning, memory and executive functioning in children. Perseveration, or the failure to respond adaptively to changing contingencies, is a hallmark on neurobehavioral assessment tasks for human fetal alcohol spectrum disorder (FASD). Adaptive responding is predominantly a product of the medial prefrontal cortex (mPFC) and is regulated by corticosteroids. In our mouse model of PAE we recently reported deficits in hippocampal formation-dependent learning and memory and a dysregulation of hippocampal formation glucocorticoid receptor (GR) subcellular distribution. Here, we examined the effect of PAE on frontal cortical-dependent behavior, as well as mPFC GR subcellular distribution and the levels of regulators of intracellular GR transport. PAE mice displayed significantly reduced response flexibility in a Y-maze reversal learning task. While the levels of total nuclear GR were reduced in PAE mPFC, levels of GR phosphorylated at serines 203, 211 and 226 were not significantly changed. Cytosolic, but not nuclear, MR levels were elevated in the PAE mPFC. The levels of critical GR trafficking proteins, FKBP51, Hsp90, cyclophilin 40, dynamitin and dynein intermediate chain, were altered in PAE mice, in favor of the exclusion of GR from the nucleus, indicating dysregulation of GR trafficking. Our findings suggest that there may be a link between a deficit in GR nuclear localization and frontal cortical learning deficits in prenatal alcohol-exposed mice.
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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.