ArticleNeuropharmacology2020
Withdrawal from chronic ethanol exposure increases postsynaptic glutamate function of insular cortex projections to the rat basolateral amygdala.
Article in Neuropharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
25 citing papers in PubMed, 40 citations in OpenAlex.
- Acute ethanol inhibits asynchronous glutamate release from mouse basolateral amygdala synapses.Neuropharmacology · 2026Article
- Chronic Intermittent Ethanol and Withdrawal Suppress Evoked and Spontaneous GABA Release Onto Distinct Populations of Basolateral Amygdala Principal Neurons.Addiction biology · 2025Article
- Multi-Target Protective Effects of β-Caryophyllene (BCP) at the Intersection of Neuroinflammation and Neurodegeneration.International journal of molecular sciences · 2025Article
- Insula under the influence: Alcohol-induced changes in resting state functional connectivity.Alcohol, clinical & experimental research · 2025Article
- Life-threatening risk factors contribute to the development of diseases with the highest mortality through the induction of regulated necrotic cell death.Cell death & disease · 2025Review
- Retrieval of an Ethanol-Conditioned Taste Aversion Promotes GABAergic Plasticity in the Anterior Insular Cortex.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Adolescent Alcohol and the Spectrum of Cognitive Dysfunction in Aging.Advances in experimental medicine and biology · 2025Review
- Epigenetic drugs and psychedelics as emerging therapies for alcohol use disorder: insights from preclinical studies.Journal of neural transmission (Vienna, Austria : 1996) · 2024Review
- Retrieval of an ethanol-conditioned taste aversion promotes GABAergic plasticity in the insular cortex.bioRxiv : the preprint server for biology · 2024Article
- Nutritional ketosis as treatment for alcohol withdrawal symptoms in female C57BL/6J mice.Scientific reports · 2024Article
- Insula Dynorphin and Kappa Opioid Receptor Systems Regulate Alcohol Drinking in a Sex-Specific Manner in Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 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
- Behavioral and biochemical effects of alcohol withdrawal in female C3H/HeNRj and C57BL/6JRj mice.Frontiers in behavioral neuroscience · 2023Article
- Protracted abstinence in males with an opioid use disorder: partial recovery of nucleus accumbens function.Translational psychiatry · 2022Article
- Structural, functional, and behavioral significance of sex and gonadal hormones in the basolateral amygdala: A review of preclinical literature.Alcohol (Fayetteville, N.Y.) · 2022Review
- Site-Specific Regulation of Stress Responses Along the Rostrocaudal Axis of the Insular Cortex in Rats.Frontiers in neuroscience · 2022Article
- Chronic Alcohol Dysregulates Glutamatergic Function in the Basolateral Amygdala in a Projection-and Sex-Specific Manner.Frontiers in cellular neuroscience · 2022Article
- Better living through understanding the insula: Why subregions can make all the difference.Neuropharmacology · 2021Review
- Ethanol modulation of cortico-basolateral amygdala circuits: Neurophysiology and behavior.Neuropharmacology · 2021Review
- Moderate adolescent chronic intermittent ethanol exposure sex-dependently disrupts synaptic transmission and kappa opioid receptor function in the basolateral amygdala of adult rats.Neuropharmacology · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
A key feature of alcohol use disorder (AUD) is negative affect during withdrawal, which often contributes to relapse and is thought to be caused by altered brain function, especially in circuits that are important mediators of emotional behaviors. Both the agranular insular cortex (AIC) and the basolateral amygdala (BLA) regulate emotions and are sensitive to ethanol-induced changes in synaptic plasticity. The AIC and BLA are reciprocally connected; and the effects of chronic ethanol exposure on this circuit have yet to be explored. Here, we use a combination of optogenetics and electrophysiology to examine the pre- and postsynaptic changes that occur to AIC-BLA synapses following withdrawal from 7- or 10-days of chronic intermittent ethanol (CIE) exposure. While CIE/withdrawal did not alter presynaptic glutamate release probability from AIC inputs, withdrawal from 10, but not 7, days of CIE increased AMPA receptor-mediated postsynaptic function at these synapses. Additionally, NMDA receptor-mediated currents evoked by electrical stimulation of the external capsule, which contains AIC afferents, were also increased during withdrawal. Notably, a single subanesthetic dose of ketamine administered at the onset of withdrawal prevented the withdrawal-induced increases in both AMPAR and NMDAR postsynaptic function. Ketamine also prevented the withdrawal-induced increases in anxiety-like behavior measured using the elevated zero maze. Together, these findings suggest that chronic ethanol exposure increases postsynaptic function within the AIC-BLA circuit and that ketamine can prevent ethanol withdrawal-induced alterations in synaptic plasticity and negative affect.
Indexed as
Identifiers
What OpenQuestion holds
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.