ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2005
Developmentally regulated actions of alcohol on hippocampal glutamatergic transmission.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 96 citations in OpenAlex.
- Synaptic Effects Induced by Alcohol.Current topics in behavioral neurosciences · 2025Review
- Review
- Ethanol interaction with α3β4 nicotinic acetylcholine receptors in neurons of the laterodorsal tegmentum.Alcoholism, clinical and experimental research · 2021Article
- Effects of Ethanol on Synaptic Plasticity and NMDA Currents in the Juvenile Rat Dentate Gyrus.Brain plasticity (Amsterdam, Netherlands) · 2020Article
- Neonatal ethanol exposure triggers apoptosis in the murine retrosplenial cortex: Role of inhibition of NMDA receptor-driven action potential firing.Neuropharmacology · 2020Article
- Distinct functions of endogenous cannabinoid system in alcohol abuse disorders.British journal of pharmacology · 2019Review
- Modulation of Gpr39, a G-protein coupled receptor associated with alcohol use in non-human primates, curbs ethanol intake in mice.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2019Article
- Effect of Alcohol on Hippocampal-Dependent Plasticity and Behavior: Role of Glutamatergic Synaptic Transmission.Frontiers in behavioral neuroscience · 2019Review
- Prenatal Alcohol Exposure Increases Histamine HAlcoholism, clinical and experimental research · 2018Article
- Synaptic targets: Chronic alcohol actions.Neuropharmacology · 2017Review
- Titrating Tipsy Targets: The Neurobiology of Low-Dose Alcohol.Trends in pharmacological sciences · 2017Review
- Third Trimester Equivalent Alcohol Exposure Reduces Modulation of Glutamatergic Synaptic Transmission by 5-HT1A Receptors in the Rat Hippocampal CA3 Region.Frontiers in neuroscience · 2016Article
- Ethanol exposure during the third trimester equivalent does not affect GABAA or AMPA receptor-mediated spontaneous synaptic transmission in rat CA3 pyramidal neurons.Journal of negative results in biomedicine · 2015Article
- Fetal Alcohol Spectrum Disorder: Potential Role of Endocannabinoids Signaling.Brain sciences · 2015Review
- Protection of the developing brain with anthocyanins against ethanol-induced oxidative stress and neurodegeneration.Molecular neurobiology · 2015Article
- Article
- Long-term genomic and epigenomic dysregulation as a consequence of prenatal alcohol exposure: a model for fetal alcohol spectrum disorders.Frontiers in genetics · 2014Review
- Neural mechanisms of pain and alcohol dependence.Pharmacology, biochemistry, and behavior · 2013Review
- Potential substrates for nicotine and alcohol interactions: a focus on the mesocorticolimbic dopamine system.Biochemical pharmacology · 2013Review
- Anandamide-CB1 receptor signaling contributes to postnatal ethanol-induced neonatal neurodegeneration, adult synaptic, and memory deficits.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
Ethanol exposure during fetal development is a leading cause of learning disabilities. Studies suggest that it alters learning and memory by permanently damaging the hippocampus. It is generally assumed that this is mediated, in part, via alterations in glutamatergic transmission. Although NMDA receptors are presumed to be the most sensitive targets of ethanol in immature neurons, this issue has not been explored in the developing hippocampus. We performed whole-cell patch-clamp recordings in hippocampal slices from neonatal rats. Unexpectedly, we found that acute ethanol (10-50 mM) exposure depresses inward currents elicited by local application of exogenous AMPA, but not NMDA, in CA3 pyramidal neurons. These findings revealed a direct effect of ethanol on postsynaptic AMPA receptors. Ethanol significantly decreased the amplitude of both AMPA and NMDA receptor-mediated EPSCs evoked by electrical stimulation. This effect was associated with an increase in the paired-pulse ratio and a decrease in the frequency of miniature EPSCs driven by depolarization of axonal terminals. These findings demonstrate that ethanol also acts at the presynaptic level. Omega-conotoxin-GVIA occluded the effect of ethanol on NMDA EPSCs, indicating that ethanol decreases glutamate release via inhibition of N-type voltage-gated Ca2+ channels. In more mature rats, ethanol did not affect the probability of glutamate release or postsynaptic AMPA receptor-mediated currents, but it did inhibit NMDA-mediated currents. We conclude that the mechanism by which ethanol inhibits glutamatergic transmission is age dependent and challenge the view that postsynaptic NMDA receptors are the primary targets of ethanol early in development.
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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.