ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2016
Chronic Intermittent Ethanol Exposure Enhances the Excitability and Synaptic Plasticity of Lateral Orbitofrontal Cortex Neurons and Induces a Tolerance to the Acute Inhibitory Actions of Ethanol.
Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.
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Who cites it
76 citing papers in PubMed, 108 citations in OpenAlex.
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- Activation by Alcohol of Prefrontal Layer 5 Pyramidal Neurons Depends on Ascending Dopaminergic Input.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- Electrophysiological sexual dimorphism as an early risk marker of alcohol use in adolescence: A longitudinal neuroimaging study.Addiction (Abingdon, England) · 2026Article
- BDNF in ventrolateral orbitofrontal cortex to dorsolateral striatum circuit moderates alcohol consumption, seeking and relapse.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026Article
- Alcohol effects on associative and sensorimotor cortico-thalamo-basal ganglia circuits alter decision making and alcohol intake.Alcohol (Fayetteville, N.Y.) · 2025Review
- Effect of an astrocyte calcium exporter on orbitofrontal cortex neuron excitability, astrocyte-synaptic interaction, and alcohol consumption.Neuropharmacology · 2025Article
- KAlcohol (Fayetteville, N.Y.) · 2025Article
- Effects of chronic ethanol exposure on dorsal medial striatal neurons receiving convergent inputs from the orbitofrontal cortex and basolateral amygdala.Neuropharmacology · 2025Article
- Synaptic Effects Induced by Alcohol.Current topics in behavioral neurosciences · 2025Review
- Alcohol, flexible behavior, and the prefrontal cortex: Functional changes underlying impaired cognitive flexibility.Neuropharmacology · 2024Review
- Home cage voluntary alcohol consumption increases binge drinking without affecting abstinence-related depressive-like behaviors or operant responding in crossed high alcohol-preferring mice (cHAPs).Alcohol (Fayetteville, N.Y.) · 2024Article
- Proactive Versus Reactive Control Strategies Differentially Mediate Alcohol Drinking in Male Wistars and P Rats.eNeuro · 2024Article
- Cross-species epigenetic regulation of nucleus accumbens KCNN3 transcripts by excessive ethanol drinking.Translational psychiatry · 2023Article
- Adaptor protein complex 2 in the orbitofrontal cortex predicts alcohol use disorder.Molecular psychiatry · 2023Article
- Chronic alcohol exposure alters action control via hyperactive premotor corticostriatal activity.Cell reports · 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
- Rapid and Chronic Ethanol Tolerance Are Composed of Distinct Memory-Like States inThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Tauopathy and alcohol consumption interact to alter locus coeruleus excitatory transmission and excitability in male and female mice.Alcohol (Fayetteville, N.Y.) · 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
16 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Alcoholism is associated with changes in brain reward and control systems, including the prefrontal cortex. In prefrontal areas, the orbitofrontal cortex (OFC) has been suggested to have an important role in the development of alcohol-abuse disorders and studies from this laboratory demonstrate that OFC-mediated behaviors are impaired in alcohol-dependent animals. However, it is not known whether chronic alcohol (ethanol) exposure alters the fundamental properties of OFC neurons. In this study, mice were exposed to repeated cycles of chronic intermittent ethanol (CIE) exposure to induce dependence and whole-cell patch-clamp electrophysiology was used to examine the effects of CIE treatment on lateral OFC (lOFC) neuron excitability, synaptic transmission, and plasticity. Repeated cycles of CIE exposure and withdrawal enhanced current-evoked action potential (AP) spiking and this was accompanied by a reduction in the after-hyperpolarization and a decrease in the functional activity of SK channels. CIE mice also showed an increase in the AMPA/NMDA ratio, and this was associated with an increase in GluA1/GluA2 AMPA receptor expression and a decrease in GluN2B NMDA receptor subunits. Following CIE treatment, lOFC neurons displayed a persistent long-term potentiation of glutamatergic synaptic transmission following a spike-timing-dependent protocol. Lastly, CIE treatment diminished the inhibitory effect of acute ethanol on AP spiking of lOFC neurons and reduced expression of the GlyT1 transporter. Taken together, these results suggest that chronic exposure to ethanol leads to enhanced intrinsic excitability and glutamatergic synaptic signaling of lOFC neurons. These alterations may contribute to the impairment of OFC-dependent behaviors in alcohol-dependent individuals.
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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.