ArticleNature neuroscience2020
Kcnn2 blockade reverses learning deficits in a mouse model of fetal alcohol spectrum disorders.
Article in Nature neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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The trial behind it
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Who cites it
23 citing papers in PubMed, 48 citations in OpenAlex.
- ACSS2 mediates prenatal alcohol exposure-related morphological and behavioral phenotypes.Neurobiology of disease · 2026Article
- Prenatal alcohol exposure perturbs the development of radial glial cells in the fetal olfactory bulb.Alcohol, clinical & experimental research · 2025Article
- Intranasal Administration of KCNN2 Blocking Peptide Improves Deficits in Cognitive Flexibility in Mouse Model of Fetal Alcohol Spectrum Disorders.The international journal of neuropsychopharmacology · 2025Article
- Reduction of APOE accounts for neurobehavioral deficits in fetal alcohol spectrum disorders.Molecular psychiatry · 2024Article
- Identification of a Hippocampus-to-Zona Incerta Projection involved in Motor Learning.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Exercise reduces physical alterations in a rat model of fetal alcohol spectrum disorders.Biological research · 2024Article
- Novel Interventions on Comorbidities in Patients with Fetal Alcohol Spectrum Disorder (FASD): An Integrative Review.Biomedicines · 2024Review
- Effects of prenatal alcohol exposure on the olfactory system development.Frontiers in neural circuits · 2024Review
- Alternative splicing events as peripheral biomarkers for motor learning deficit caused by adverse prenatal environments.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- 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
- Review
- Fatty acid metabolism changes in association with neurobehavioral deficits in animal models of fetal alcohol spectrum disorders.Communications biology · 2023Article
- Sensory Motor Function Disturbances in Mice Prenatally Exposed to Low Dose of Ethanol: A Neurobehavioral Study in Postnatal and Adult Stages.Neurology international · 2023Article
- Fetal alcohol spectrum disorders.Nature reviews. Disease primers · 2023Review
- Domesticated HERV-W env contributes to the activation of the small conductance CaVirologica Sinica · 2023Article
- Caspase-3 Inhibition toward Perinatal Protection of the Developing Brain from Environmental Stress.Developmental neuroscience · 2023Review
- Article
- Activation of the anterior cingulate cortex ameliorates anxiety in a preclinical model of fetal alcohol spectrum disorders.Translational psychiatry · 2022Article
- Identification of the Novel Gene Markers Based on the Gene Profile among Different Severity of Obstructive Sleep Apnea.Computational and mathematical methods in medicine · 2022Article
- Transgenerational Effects of Prenatal Ethanol Exposure in Prepubescent Mice.Frontiers in cell and developmental biology · 2022Article
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Authors and funding
17 authors at 4 institutions in 3 countries.
Funding
Abstract
Learning disabilities are hallmarks of congenital conditions caused by prenatal exposure to harmful agents. These include fetal alcohol spectrum disorders (FASDs) with a wide range of cognitive deficiencies, including impaired motor skill development. Although these effects have been well characterized, the molecular effects that bring about these behavioral consequences remain to be determined. We previously found that the acute molecular responses to alcohol in the embryonic brain are stochastic, varying among neural progenitor cells. However, the pathophysiological consequences stemming from these heterogeneous responses remain unknown. Here we show that acute responses to alcohol in progenitor cells altered gene expression in their descendant neurons. Among the altered genes, an increase of the calcium-activated potassium channel Kcnn2 in the motor cortex correlated with motor learning deficits in a mouse model of FASD. Pharmacologic blockade of Kcnn2 improves these learning deficits, suggesting Kcnn2 blockers as a new intervention for learning disabilities in FASD.
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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.