ArticlePsychopharmacology2016
Social stress-escalated intermittent alcohol drinking: modulation by CRF-R1 in the ventral tegmental area and accumbal dopamine in mice.
Article in Psychopharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 60 citations in OpenAlex.
- Individualized assignment to short-term alcohol abstinence: A proof-of-concept human laboratory study using psychopathology dimensions.Drug and alcohol dependence reports · 2026Article
- The influence of stress and social defeat on neurobiological reinforcement mechanisms across reward to withdrawal in nicotine addiction.Psychopharmacology · 2025Review
- Concurrent consumption of ethanol and corticosterone during adolescence alters neuroimmune sensitivity in Sprague Dawley rats.Addiction neuroscience · 2025Article
- Voluntary wheel running during adolescence prevents the increase in ethanol intake induced by social defeat in male mice.Psychopharmacology · 2025Article
- Neurokinin-1 receptors in the nucleus accumbens shell influence sensitivity to social defeat stress and stress-induced alcohol consumption in male mice.Addiction neuroscience · 2024Article
- Sex differences in neural response to an acute stressor in individuals with an alcohol use disorder.Alcohol, clinical & experimental research · 2024Article
- Article
- Prior experience with flavored alcohol increases preference for flavored alcohol but flavor does not influence binge-like drinking behavior in mice.Physiology & behavior · 2023Article
- Reinstatement of Pavlovian responses to alcohol cues by stress.Psychopharmacology · 2023Article
- Vicarious Social Defeat Increases Conditioned Rewarding Effects of Cocaine and Ethanol Intake in Female Mice.Biomedicines · 2023Article
- Corticotropin releasing factor and drug seeking in substance use disorders: Preclinical evidence and translational limitations.Addiction neuroscience · 2022Article
- Actions of feeding-related peptides on the mesolimbic dopamine system in regulation of natural and drug rewards.Addiction neuroscience · 2022Article
- Opposite effects of stress on effortful motivation in high and low anxiety are mediated by CRHR1 in the VTA.Science advances · 2022Article
- Repeated cocaine or methamphetamine treatment alters astrocytic CRF2 and GLAST expression in the ventral midbrain.Addiction biology · 2022Article
- Friend of the Devil: Negative Social Influences Driving Substance Use Disorders.Frontiers in behavioral neuroscience · 2022Review
- Neurobiological Bases of Alcohol Consumption After Social Stress.Current topics in behavioral neurosciences · 2022Article
- FACTORS CONTRIBUTING TO THE ESCALATION OF ALCOHOL CONSUMPTION.Neuroscience and biobehavioral reviews · 2022Review
- Ethanol intake in male mice exposed to social defeat: Environmental enrichment potentiates resilience.Neurobiology of stress · 2021Article
- Hypoactive Thalamic Crh+ Cells in a Female Mouse Model of Alcohol Drinking After Social Trauma.Biological psychiatry · 2021Article
- Oxytocin Signaling as a Target to Block Social Defeat-Induced Increases in Drug Abuse Reward.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
rationaleExcessive alcohol (EtOH) drinking is difficult to model in animals despite the extensive human literature demonstrating that stress increases EtOH consumption.
objectiveThe current experiments show escalations in voluntary EtOH drinking caused by a history of social defeat stress and intermittent access to EtOH in C57BL/6J mice compared to non-stressed mice given intermittent EtOH or continuous EtOH. To explore a mechanistic link between stress and drinking, we studied the role of corticotropin-releasing factor type-1 receptors (CRF-R1) in the dopamine-rich ventral tegmental area (VTA).
resultsIntra-VTA infusions of a CRF-R1 antagonist, CP376395, infused into the VTA dose-dependently and selectively reduced intermittent EtOH intake in stressed and non-stressed mice, but not in mice given continuous EtOH. In contrast, intra-VTA infusions of the CRF-R2 antagonist astressin2B non-specifically suppressed both EtOH and H2O drinking in the stressed group without effects in the non-stressed mice. Using in vivo microdialysis in the nucleus accumbens (NAc) shell, we observed that stressed mice drinking EtOH intermittently had elevated levels of tonic dopamine concentrations compared to non-stressed drinking mice. Also, VTA CP376395 potentiated dopamine output to the NAc only in the stressed group causing further elevations of dopamine post-infusion.
conclusionsThese findings illustrate a role for extrahypothalamic CRF-R1 as especially important for stress-escalated EtOH drinking beyond schedule-escalated EtOH drinking. CRF-R1 may be a mechanism for balancing the dysregulation of stress and reward in alcohol use disorders.
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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.