ArticleAlcoholism, clinical and experimental research2019
Chronic Ethanol Exposure and Withdrawal Impair Synaptic GABA
Article in Alcoholism, clinical and experimental research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.
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Who cites it
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.
- Probiotics-role in alleviating the impact of alcohol liver disease and alcohol deaddiction: a systematic review.Frontiers in nutrition · 2024Pooled it
- Multi-omics and electrophysiological examination of GABAMolecular psychiatry · 2026Article
- Chronic ethanol exposure reduces resting state functional connectivity and regional synchrony in male rats.Psychopharmacology · 2026Article
- Prenatal alcohol exposure dysregulates the expression of clock genes and alters rhythmic behaviour in mice.Open biology · 2025Article
- Chronic ethanol exposure produces long-lasting, subregion-specific physiological adaptations in RMTg-projecting mPFC neurons.Neuropharmacology · 2024Article
- Effects of combined exposure to ethanol and delta-9-tetrahydrocannabinol during adolescence on synaptic plasticity in the prefrontal cortex of Long Evans rats.Neuropharmacology · 2024Article
- Divergent Population-Specific Effects of Chronic Ethanol Exposure on Excitability and Inhibitory Transmission in Male and Female Rat Central Amygdala.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Article
- Chronic ethanol induces a pro-inflammatory switch in interleukin-1β regulation of GABAergic signaling in the medial prefrontal cortex of male mice.Brain, behavior, and immunity · 2023Article
- Pharmacological administration of 3α,5α-THP into the nucleus accumbens core increases 3α,5α-THP expression and reduces alcohol self-administration.Alcohol, clinical & experimental research · 2023Article
- GABAergic signaling in alcohol use disorder and withdrawal: pathological involvement and therapeutic potential.Frontiers in neural circuits · 2023Review
- Modulation of neuronal excitability by binge alcohol drinking.Frontiers in molecular neuroscience · 2023Review
- Comorbidity of Post-Traumatic Stress Disorder and Alcohol Use Disorder: Animal Models and Associated Neurocircuitry.International journal of molecular sciences · 2022Review
- GABACells · 2022Article
- Medial prefrontal cortex-basolateral amygdala circuit dysfunction in chronic alcohol-exposed male rats.Neuropharmacology · 2022Article
- Targeting prefrontal cortex GABAergic microcircuits for the treatment of alcohol use disorder.Frontiers in synaptic neuroscience · 2022Review
- 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
- Somatostatin neurons control an alcohol binge drinking prelimbic microcircuit in mice.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2021Article
- Increased Synaptic Strength and mGluAlcoholism, clinical and experimental research · 2021Article
- Histone modifications, DNA methylation, and the epigenetic code of alcohol use disorder.International review of neurobiology · 2021Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
backgroundThe prefrontal cortex (PFC) acts as an integrative hub for the processing of cortical and subcortical input into meaningful efferent signaling, permitting complex associative behaviors. PFC dysfunction is consistently observed with ethanol (EtOH) dependence and is a core component of the pathology of alcohol use disorders in current models of addiction. While intracortical gamma-aminobutryric acid (GABA)ergic neurotransmission is understood to be essential for maintaining coordinated network activity within the cortex, relatively little is known regarding functional GABAergic adaptations in PFC during EtOH dependence.
methodsIn the present study, male and female (> postnatal day 60) Sprague-Dawley rats were administered EtOH (5.0 g/kg; intragastric gavage) for 14 to 15 consecutive days. Twenty-four hours after the final administration, animals were sacrificed and brains extracted for electrophysiological recordings of isolated GABA
resultsChronic EtOH exposure significantly attenuated activity-dependent spontaneous GABA
conclusionsTaken together, these results demonstrate that chronic EtOH exposure impairs synaptic inhibitory neurotransmission in deep-layer pyramidal neurons of the medial PFC in both male and female rats. These maladaptations occur in neurons projecting to numerous regions implicated in the sequelae of EtOH dependence, offering a mechanistic link between the manifestation of PFC dysfunction and negative affective states observed with extended consumption.
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