ArticleAlcoholism, clinical and experimental research2019
Amygdala Arginine Vasopressin Modulates Chronic Ethanol Withdrawal Anxiety-Like Behavior in the Social Interaction Task.
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 14 papers.
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14 citing papers in PubMed, 20 citations in OpenAlex.
- Adolescent ethanol exposure reduces central amygdala GABA transmission but preserves noradrenergic signaling in adulthood.Neuropharmacology · 2026Article
- Sex-dependent effects of ethanol withdrawal from a single- and repeated binge episode exposures on social anxiety-like behavior and neuropeptide gene expression in adolescent rats.Alcohol (Fayetteville, N.Y.) · 2025Article
- Stay social, stay young: a bioanthropological outlook on the processes linking sociality and ageing.GeroScience · 2025Review
- The Relationship Between Oxytocin and Alcohol Dependence.Current topics in behavioral neurosciences · 2025Review
- Chronic alcohol withdrawal-associated increases in VTAAdvances in drug and alcohol research · 2025Article
- Prenatal allergic inflammation in rats confers sex-specific alterations to oxytocin and vasopressin innervation in social brain regions.Hormones and behavior · 2024Article
- The Role of Oxytocin and Vasopressin in Drug-Induced Reward-Implications for Social and Non-Social Factors.Biomolecules · 2023Review
- Modulation of social behavior by distinct vasopressin sources.Frontiers in endocrinology · 2023Review
- Impact of adolescent intermittent ethanol exposure in male and female rats on social drinking and neuropeptide gene expression.Alcoholism, clinical and experimental research · 2022Article
- Tetratricopeptide repeat domain 9A knockout induces social anxiety and impairs offense behaviors in female mice.Iranian journal of basic medical sciences · 2022Article
- Oxytocin and vasopressin: Signalling, behavioural modulation and potential therapeutic effects.British journal of pharmacology · 2022Review
- Friend of the Devil: Negative Social Influences Driving Substance Use Disorders.Frontiers in behavioral neuroscience · 2022Review
- The Basolateral Amygdala to Ventral Hippocampus Circuit Controls Anxiety-Like Behaviors Induced by Morphine Withdrawal.Frontiers in cellular neuroscience · 2022Article
- Chemogenetic Inactivation of Orbitofrontal Cortex Decreases Cue-induced Reinstatement of Ethanol and Sucrose Seeking in Male and Female Wistar Rats.Alcoholism, clinical and experimental research · 2020Article
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7 authors at 1 institution in 1 country.
Funding
Abstract
backgroundChronic ethanol (EtOH) exposure induces neurobehavioral maladaptations in the brain though the precise changes have not been fully explored. The central nucleus of the amygdala (CEA) regulates anxiety-like behavior induced by withdrawal from chronic intermittent EtOH (CIE) exposure, and the arginine vasopressin (AVP) system within the CEA regulates many anxiety-like behaviors. Thus, adaptations occur in the CEA AVP system due to chronic EtOH exposure, which lead to anxiety-like behaviors in rats.
methodsChronic exposure to a low-dose EtOH (4.5% wt/vol) induces anxiety-like behavior in rats. Wistar or Sprague Dawley rats were exposed to a modified CIE or CIE, while intra-CEA microinjections of AVP or a V1b receptor antagonist were used to elicit or block withdrawal-induced anxiety. Additionally, AVP microinjections into the CEA were given 24 hours following 15 days of continuous high-dose EtOH (7% wt/vol), a time period when rats no longer express anxiety. Chemogenetics was also used to activate the basolateral amygdala (BLA) or deactivate the dorsal periaqueductal gray=(dm/dlPAG) therefore PAG=periaqueductal gray to elicit or block withdrawal-induced anxiety.
resultsAVP microinjected into the CEA in lieu of exposure to the first 2 cycles of CIE was sufficient to induce anxiety-like behavior in these commonly used rat strains. The V1b receptor antagonist, but not an oxytocin receptor agonist, into the CEA during the first 2 withdrawal cycles suppressed anxiety. However, activation of the BLA in lieu of exposure to the first 2 cycles of CIE was insufficient to induce anxiety-like behavior. AVP microinjection into the CEA 24 hours into withdrawal reelicited anxiety-like behavior, and deactivation of the dm/dlPAG reduced this effect of CEA AVP.
conclusionsTaken together, this study demonstrates a role of CEA AVP and a CEA-dm/dlPAG circuit in the development of anxiety induced by CIE. Such information is valuable for identifying novel therapeutic targets for alcohol- and anxiety-associated disorders.
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