ArticleThe Journal of pharmacology and experimental therapeutics2011
Chronic ethanol and withdrawal differentially modulate lateral/basolateral amygdala paracapsular and local GABAergic synapses.
Article in The Journal of pharmacology and experimental therapeutics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
What it found
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Who cites it
48 citing papers in PubMed, 67 citations in OpenAlex.
- Cannabidiol mitigates alcohol dependence and withdrawal with neuroprotective effects in the basolateral amygdala and striatum.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026Article
- Chronic Intermittent Ethanol and Withdrawal Suppress Evoked and Spontaneous GABA Release Onto Distinct Populations of Basolateral Amygdala Principal Neurons.Addiction biology · 2025Article
- Age- and cytokine-dependent modulation of GABAergic transmission within the basolateral amygdala of male Sprague Dawley rats.Neuropharmacology · 2025Article
- A role for circuitry of the cortical amygdala in excessive alcohol drinking, withdrawal, and alcohol use disorder.Alcohol (Fayetteville, N.Y.) · 2024Review
- Toluene alters the intrinsic excitability and excitatory synaptic transmission of basolateral amygdala neurons.Frontiers in neuroscience · 2024Article
- Sex differences in stress-induced alcohol intake: a review of preclinical studies focused on amygdala and inflammatory pathways.Psychopharmacology · 2022Review
- Structural, functional, and behavioral significance of sex and gonadal hormones in the basolateral amygdala: A review of preclinical literature.Alcohol (Fayetteville, N.Y.) · 2022Review
- The Synaptic Interactions of Alcohol and the Endogenous Cannabinoid System.Alcohol research : current reviews · 2022Review
- 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
- Chronic Ethanol Exposure Potentiates Cholinergic Neurotransmission in the Basolateral Amygdala.Neuroscience · 2021Article
- Role of Hippocampal Neurogenesis in Alcohol Withdrawal Seizures.Brain plasticity (Amsterdam, Netherlands) · 2020Review
- Withdrawal from chronic ethanol exposure increases postsynaptic glutamate function of insular cortex projections to the rat basolateral amygdala.Neuropharmacology · 2020Article
- Brain-wide functional architecture remodeling by alcohol dependence and abstinence.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Article
- Chronic Intermittent Ethanol Exposure Selectively Increases Synaptic Excitability in the Ventral Domain of the Rat Hippocampus.Neuroscience · 2019Article
- The center of the emotional universe: Alcohol, stress, and CRF1 amygdala circuitry.Alcohol (Fayetteville, N.Y.) · 2018Review
- Oxytocin and vasopressin modulation of social anxiety following adolescent intermittent ethanol exposure.Psychopharmacology · 2018Article
- SNARE Complex-Associated Proteins in the Lateral Amygdala of Macaca mulatta Following Long-Term Ethanol Drinking.Alcoholism, clinical and experimental research · 2018Article
- Synaptic plasticity mechanisms common to learning and alcohol use disorder.Learning & memory (Cold Spring Harbor, N.Y.) · 2018Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Withdrawal-related anxiety is cited as a major contributor to relapse in recovering alcoholics. Changes in lateral/basolateral amygdala (BLA) neurotransmission could directly influence anxiety-like behaviors after chronic ethanol exposure and withdrawal. We have shown that these treatments enhance BLA glutamatergic function and neurotransmission. However, the BLA GABAergic system tightly controls the expression of anxiety-like behavior, and additional neuroadaptations in this system are potentially important as well. The intrinsic BLA GABAergic system consists of at least two populations of interneurons: local feed-back interneurons scattered throughout the region and feed-forward interneurons concentrated within groups found in the lateral/paracapsular region of the BLA. In the present study, we found that withdrawal from chronic ethanol robustly decreased presynaptic function at feed-forward GABA synapses but did not alter neurotransmitter release from local interneurons. Differential presynaptic changes at these synapses were complemented by decreased zolpidem sensitivity at feed-forward synapses and decreased midazolam sensitivity at local synapses. Consistent with this, chronic ethanol/withdrawal decreased expression of GABA α1-subunit total protein and increased surface expression of α4-subunit protein. We also found transient increases in GABA-receptor-associated protein levels and persistent increases in γ2-subunit and gephyrin proteins that would suggest alterations in GABA(A) receptor trafficking that might help regulate changes in α4-subunit localization. These data together suggest that chronic ethanol and withdrawal differentially modulate local and lateral paracapsular cell GABAergic synapses via distinct presynaptic and postsynaptic mechanisms. These findings extend our understanding of the neurobiological mechanisms governing changes in anxiety-like behavior after chronic ethanol exposure and withdrawal.
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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.