ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2013
Ethanol reduces neuronal excitability of lateral orbitofrontal cortex neurons via a glycine receptor dependent mechanism.
Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed, 76 citations in OpenAlex.
- Deleterious effects of a low amount of ethanol on LTP-like plasticity in human cortex.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2014Trial
- Article
- Effect of an astrocyte calcium exporter on orbitofrontal cortex neuron excitability, astrocyte-synaptic interaction, and alcohol consumption.Neuropharmacology · 2025Article
- Synaptic Effects Induced by Alcohol.Current topics in behavioral neurosciences · 2025Review
- Short- and Long-Term High-Fat Diet Exposure Differentially Alters Phasic and Tonic GABAergic Signaling onto Lateral Orbitofrontal Pyramidal Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Long-term effects of low prenatal alcohol exposure on GABAergic interneurons of the murine posterior parietal cortex.Alcohol, clinical & experimental research · 2023Article
- Adaptor protein complex 2 in the orbitofrontal cortex predicts alcohol use disorder.Molecular psychiatry · 2023Article
- Chronic intermittent ethanol exposure differentially alters the excitability of neurons in the orbitofrontal cortex and basolateral amygdala that project to the dorsal striatum.Neuropharmacology · 2023Article
- Modulation of neuronal excitability by binge alcohol drinking.Frontiers in molecular neuroscience · 2023Review
- The ethanol inhibition of basolateral amygdala neuron spiking is mediated by a γ-aminobutyric acid type A-mediated tonic current.Alcoholism, clinical and experimental research · 2022Article
- Orbitofrontal cortex subregion inhibition during binge-like and aversion-resistant alcohol drinking.Alcohol (Fayetteville, N.Y.) · 2022Article
- Targeting prefrontal cortex GABAergic microcircuits for the treatment of alcohol use disorder.Frontiers in synaptic neuroscience · 2022Review
- Prenatal Drugs and Their Effects on the Developing Brain: Insights From Three-Dimensional Human Organoids.Frontiers in neuroscience · 2022Review
- Understanding ethanol's acute effects on medial prefrontal cortex neural activity using state-space approaches.Neuropharmacology · 2021Review
- Ethanol modulation of cortico-basolateral amygdala circuits: Neurophysiology and behavior.Neuropharmacology · 2021Review
- Alcohol reduces the activity of somatostatin interneurons in the mouse prefrontal cortex: A neural basis for its disinhibitory effect?Neuropharmacology · 2021Article
- Ethanol Alters Variability, But Not Rate, of Firing in Medial Prefrontal Cortex Neurons of Awake-Behaving Rats.Alcoholism, clinical and experimental research · 2020Article
- Moderate prenatal alcohol exposure alters the number and function of GABAergic interneurons in the murine orbitofrontal cortex.Alcohol (Fayetteville, N.Y.) · 2020Article
- Selective impact of lateral orbitofrontal cortex inactivation on reinstatement of alcohol seeking in male Long-Evans rats.Neuropharmacology · 2020Article
- Influence of nonsynaptic α1 glycine receptors on ethanol consumption and place preference.Addiction biology · 2020Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Trauma-induced damage to the orbitofrontal cortex (OFC) often results in behavioral inflexibility and impaired judgment. Human alcoholics exhibit similar cognitive deficits suggesting that OFC neurons are susceptible to alcohol-induced dysfunction. A previous study from this laboratory examined OFC mediated cognitive behaviors in mice and showed that behavioral flexibility during a reversal learning discrimination task was reduced in alcohol-dependent mice. Despite these intriguing findings, the actions of alcohol on OFC neuron function are unknown. To address this issue, slices containing the lateral OFC (lOFC) were prepared from adult C57BL/6J mice and whole-cell patch clamp electrophysiology was used to characterize the effects of ethanol (EtOH) on neuronal function. EtOH (66 mM) had no effect on AMPA-mediated EPSCs but decreased those mediated by NMDA receptors. EtOH (11-66 mM) also decreased current-evoked spike firing and this was accompanied by a decrease in input resistance and a modest hyperpolarization. EtOH inhibition of spike firing was prevented by the GABAA antagonist picrotoxin, but EtOH had no effect on evoked or spontaneous GABA IPSCs. EtOH increased the holding current of voltage-clamped neurons and this action was blocked by picrotoxin but not the more selective GABAA antagonist biccuculine. The glycine receptor antagonist strychnine also prevented EtOH's effect on holding current and spike firing, and western blotting revealed the presence of glycine receptors in lOFC. Overall, these results suggest that acutely, EtOH may reduce lOFC function via a glycine receptor dependent process and this may trigger neuroadaptive mechanisms that contribute to the impairment of OFC-dependent behaviors in alcohol-dependent subjects.
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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.