ArticleeLife2019
The NKCC1 antagonist bumetanide mitigates interneuronopathy associated with ethanol exposure in utero.
Article in eLife, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 18 citations in OpenAlex.
- Moderate prenatal alcohol exposure differentially alters acute ethanol sensitivity of GABAergic transmission in CRFR1- and CRFR1+ CeM Neurons.Addiction neuroscience · 2026Article
- Developmental alcohol exposure: Impacts on medial prefrontal cortex morphology and the excitatory-inhibitory balance.Progress in neuro-psychopharmacology & biological psychiatry · 2026Review
- The NKCC1 Antagonist Bumetanide, Administered After Prenatal Alcohol Exposure, Mitigates Ethanol-Induced Aberrance in Tangential Migration of GABAergic Interneurons in Mouse Medial Prefrontal Cortex.Alcohol, clinical & experimental research · 2026Article
- A Single Dose of a Psychedelic Drug Repairs Prefrontal Cortex Synaptic Physiology in a Mouse Model of Prenatal Alcohol Exposure.Brain and behavior · 2026Article
- The NKCC1 Inhibitor Bumetanide Restores Cortical Feedforward Inhibition and Lessens Sensory Hypersensitivity in Early Postnatal Fragile X Mice.Biological psychiatry · 2025Article
- GABA system as the cause and effect in early development.Neuroscience and biobehavioral reviews · 2024Review
- Novel Interventions on Comorbidities in Patients with Fetal Alcohol Spectrum Disorder (FASD): An Integrative Review.Biomedicines · 2024Review
- Review
- Precocious emergence of cognitive and synaptic dysfunction in 3xTg-AD mice exposed prenatally to ethanol.Alcohol (Fayetteville, N.Y.) · 2023Article
- Review
- NLRP3 inflammasome-mediated choroid plexus hypersecretion contributes to hydrocephalus after intraventricular hemorrhage via phosphorylated NKCC1 channels.Journal of neuroinflammation · 2022Article
- Pre-implantation alcohol exposure induces lasting sex-specific DNA methylation programming errors in the developing forebrain.Clinical epigenetics · 2021Article
- Enhancement of parvalbumin interneuron-mediated neurotransmission in the retrosplenial cortex of adolescent mice following third trimester-equivalent ethanol exposure.Scientific reports · 2021Article
- Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Prenatal exposure to ethanol induces aberrant tangential migration of corticopetal GABAergic interneurons, and long-term alterations in the form and function of the prefrontal cortex. We have hypothesized that interneuronopathy contributes significantly to the pathoetiology of fetal alcohol spectrum disorders (FASD). Activity-dependent tangential migration of GABAergic cortical neurons is driven by depolarizing responses to ambient GABA present in the cortical enclave. We found that ethanol exposure potentiates the depolarizing action of GABA in GABAergic cortical interneurons of the embryonic mouse brain. Pharmacological antagonism of the cotransporter NKCC1 mitigated ethanol-induced potentiation of GABA depolarization and prevented aberrant patterns of tangential migration induced by ethanol in vitro. In a model of FASD, maternal bumetanide treatment prevented interneuronopathy in the prefrontal cortex of ethanol exposed offspring, including deficits in behavioral flexibility. These findings position interneuronopathy as a mechanism of FASD symptomatology, and posit NKCC1 as a pharmacological target for the management of FASD.
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Registered trials
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