ArticleAlcoholism, clinical and experimental research2010
Ethanol acutely inhibits ionotropic glutamate receptor-mediated responses and long-term potentiation in the developing CA1 hippocampus.
Article in Alcoholism, clinical and experimental research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 54 citations in OpenAlex.
- Review
- Alcohol Enhances Responses to High Frequency Stimulation in Hippocampus from Transgenic Mice with Increased Astrocyte Expression of IL-6.Cellular and molecular neurobiology · 2021Article
- Effects of Ethanol on Synaptic Plasticity and NMDA Currents in the Juvenile Rat Dentate Gyrus.Brain plasticity (Amsterdam, Netherlands) · 2020Article
- Post-exposure environment modulates long-term developmental ethanol effects on behavior, neuroanatomy, and cortical oscillations.Brain research · 2020Article
- Neonatal ethanol exposure triggers apoptosis in the murine retrosplenial cortex: Role of inhibition of NMDA receptor-driven action potential firing.Neuropharmacology · 2020Article
- Impact of autism-associated genetic variants in interaction with environmental factors on ADHD comorbidities: an exploratory pilot study.Journal of neural transmission (Vienna, Austria : 1996) · 2019Article
- Neonatal ethanol exposure impairs long-term context memory formation and prefrontal immediate early gene expression in adolescent rats.Behavioural brain research · 2019Article
- Impairment of the context preexposure facilitation effect in juvenile rats by neonatal alcohol exposure is associated with decreased Egr-1 mRNA expression in the prefrontal cortex.Behavioral neuroscience · 2018Article
- Synaptic plasticity mechanisms common to learning and alcohol use disorder.Learning & memory (Cold Spring Harbor, N.Y.) · 2018Review
- Effects of acute alcohol on excitability in the CNS.Neuropharmacology · 2017Review
- Impact of exercise and a complex environment on hippocampal dendritic morphology, Bdnf gene expression, and DNA methylation in male rat pups neonatally exposed to alcohol.Developmental neurobiology · 2017Article
- What the Spectrum of Microglial Functions Can Teach us About Fetal Alcohol Spectrum Disorder.Frontiers in synaptic neuroscience · 2017Review
- Neurotrophins in the Brain: Interaction With Alcohol Exposure During Development.Vitamins and hormones · 2017Review
- Neonatal binge alcohol exposure increases microglial activation in the developing rat hippocampus.Neuroscience · 2016Article
- Further characterization of the effect of ethanol on voltage-gated Ca(2+) channel function in developing CA3 hippocampal pyramidal neurons.Brain research · 2016Article
- Effects of Developmental Alcohol Exposure on Potentiation and Depression of Visual Cortex Responses.Alcoholism, clinical and experimental research · 2015Article
- Effects of developmental alcohol exposure vs. intubation stress on BDNF and TrkB expression in the hippocampus and frontal cortex of neonatal rats.International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience · 2015Article
- Ethanol upregulates NMDA receptor subunit gene expression in human embryonic stem cell-derived cortical neurons.PloS one · 2015Article
- Activity and social behavior in a complex environment in rats neonatally exposed to alcohol.Alcohol (Fayetteville, N.Y.) · 2014Article
- Long-term genomic and epigenomic dysregulation as a consequence of prenatal alcohol exposure: a model for fetal alcohol spectrum disorders.Frontiers in genetics · 2014Review
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Funding
Abstract
backgroundDevelopmental ethanol (EtOH) exposure damages the hippocampus, causing long-lasting alterations in learning and memory. Alterations in glutamatergic synaptic transmission and plasticity may play a role in the mechanism of action of EtOH. This signaling is fundamental for synaptogenesis, which occurs during the third trimester of human pregnancy (first 12 days of life in rats).
methodsAcute coronal brain slices were prepared from 7- to 9-day-old rats. Extracellular and patch-clamp electrophysiological recording techniques were used to characterize the acute effects of EtOH on alpha-amino-3-hydroxyl-5-methyl-4-isoxazole-propionate receptor (AMPAR)- and N-methyl-D-aspartate receptor (NMDAR)-mediated responses and long-term potentiation (LTP) in the CA1 hippocampal region.
resultsEthanol (40 and 80 mM) inhibited AMPAR- and NMDAR-mediated field excitatory postsynaptic potentials (fEPSPs). EtOH (80 mM) also reduced AMPAR-mediated fEPSPs in the presence of an inhibitor of Ca2+ permeable AMPARs. The effect of 80 mM EtOH on NMDAR-mediated fEPSPs was significantly greater in the presence of Mg2+. EtOH (80 mM) neither affected the paired-pulse ratio of AMPAR-mediated fEPSPs nor the presynaptic volley. The paired-pulse ratio of AMPAR-mediated excitatory postsynaptic currents was not affected either, and the amplitude of these currents was inhibited to a lesser extent than that of fEPSPs. EtOH (80 mM) inhibited LTP of AMPAR-mediated fEPSPs.
conclusionsAcute EtOH exposure during the third-trimester equivalent of human pregnancy inhibits hippocampal glutamatergic transmission and LTP induction, which could alter synapse refinement and ultimately contribute to the pathophysiology of fetal alcohol spectrum disorder.
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