ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2017
Ethanol Dependence Abolishes Monoamine and GIRK (Kir3) Channel Inhibition of Orbitofrontal Cortex Excitability.
Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
34 citing papers in PubMed, 50 citations in OpenAlex.
- A randomized controlled study of the effect of ifenprodil on alcohol use in patients with alcohol dependence.Neuropsychopharmacology reports · 2018Trial
- Decoding the serotonin-alcohol crosstalk: the role of central serotonergic dysregulation in alcohol use disorder.Pharmacological reports : PR · 2026Review
- Heavy adolescent drinking makes the adult brain more vulnerable to ethanol by permanently altering the age-dependent interplay between alcohol, GIRK channels and activin.Molecular psychiatry · 2026Article
- Prefrontal Cortex 5-HT1A Receptor-Coupled Inwardly Rectifying Potassium Channels Decreased Seizure Susceptibility in Rat Models With Autism Spectrum Disorder.Neural plasticity · 2026Article
- Noradrenergic Mechanisms and Circuitry of Hyperkatifeia in Alcohol Use Disorder.Biological psychiatry · 2025Review
- Terahertz photoneuromodulation of lateral orbitofrontal cortex neurons ameliorates stress-induced depression and cognitive impairment.Fundamental research · 2025Article
- Chronic ethanol exposure in mice evokes pre- and postsynaptic deficits in GABAergic transmission in ventral tegmental area GABA neurons.British journal of pharmacology · 2025Article
- The NaeLife · 2024Article
- Neuronal-specific methylome and hydroxymethylome analysis reveal significant loci associated with alcohol use disorder.Frontiers in genetics · 2024Article
- Ethanol-Induced Suppression of G Protein-Gated Inwardly Rectifying KBiological psychiatry · 2023Article
- Neuronal-specific methylome and hydroxymethylome analysis reveal replicated and novel loci associated with alcohol use disorder.medRxiv : the preprint server for health sciences · 2023Article
- The NabioRxiv : the preprint server for biology · 2023Article
- Contingent Amygdala Inputs Trigger Heterosynaptic LTP at Hippocampus-To-Accumbens Synapses.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Neuronal G protein-gated KAmerican journal of physiology. Cell physiology · 2022Review
- Noradrenergic circuits and signaling in substance use disorders.Neuropharmacology · 2022Review
- Orbitofrontal cortex subregion inhibition during binge-like and aversion-resistant alcohol drinking.Alcohol (Fayetteville, N.Y.) · 2022Article
- Alcohol and the brain: from genes to circuits.Trends in neurosciences · 2021Review
- Suppression of pyramidal neuron G protein-gated inwardly rectifying K+ channel signaling impairs prelimbic cortical function and underlies stress-induced deficits in cognitive flexibility in male, but not female, mice.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2021Article
- Ethanol modulation of cortico-basolateral amygdala circuits: Neurophysiology and behavior.Neuropharmacology · 2021Review
- Sex- and subtype-specific adaptations in excitatory signaling onto deep-layer prelimbic cortical pyramidal neurons after chronic alcohol exposure.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2021Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Alcohol abuse disorders are associated with dysfunction of frontal cortical areas including the orbitofrontal cortex (OFC). The OFC is extensively innervated by monoamines, and drugs that target monoamine receptors have been used to treat a number of neuropsychiatric diseases, including alcoholism. However, little is known regarding how monoamines affect OFC neuron excitability or whether this modulation is altered by chronic exposure to ethanol. In this study, we examined the effect of dopamine, norepinephrine, and serotonin on lOFC neuronal excitability in naive mice and in those exposed to chronic intermittent ethanol (CIE) treatment. All three monoamines decreased current-evoked spike firing of lOFC neurons and this action required G
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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.