ArticlePsychopharmacology2015
Reduction of ethanol intake by corticotropin-releasing factor receptor-1 antagonist in "heavy-drinking" mice in a free-choice paradigm.
Article in Psychopharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 11 citations in OpenAlex.
- The center of the emotional universe: Alcohol, stress, and CRF1 amygdala circuitry.Alcohol (Fayetteville, N.Y.) · 2018Review
- Persistent escalation of alcohol consumption by mice exposed to brief episodes of social defeat stress: suppression by CRF-R1 antagonism.Psychopharmacology · 2018Article
- Interaction Between Stress and Addiction: Contributions From Latin-American Neuroscience.Frontiers in psychology · 2018Review
- Possible involvement of ACSS2 gene in alcoholism.Journal of neural transmission (Vienna, Austria : 1996) · 2017Article
- A Functional Switch in Tonic GABA Currents Alters the Output of Central Amygdala Corticotropin Releasing Factor Receptor-1 Neurons Following Chronic Ethanol Exposure.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- Serotonergic Neuroplasticity in Alcohol Addiction.Brain plasticity (Amsterdam, Netherlands) · 2016Review
- IL-1 receptor signaling in the basolateral amygdala modulates binge-like ethanol consumption in male C57BL/6J mice.Brain, behavior, and immunity · 2016Article
- An Update on CRF Mechanisms Underlying Alcohol Use Disorders and Dependence.Frontiers in endocrinology · 2016Review
- Alcohol Use Disorder Increases the Risk of Irritable Bowel Disease: A Nationwide Retrospective Cohort Study.Medicine · 2015Observational
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
rationaleWe hypothesized that the corticotropin-releasing factor (CRF) system is hyperresponsive in animals with high ethanol intake, which exhibits a reduction of ethanol intake when administered with a CRF1 receptor antagonist.
methodsOutbred Swiss mice were subjected to a long-term, three-bottle, free-choice paradigm (5 and 10 % [v/v] ethanol and water) that consisted of four phases: acquisition (AC; 10 weeks), withdrawal (W; 2 weeks), reexposure (RE; 2 weeks), and quinine-adulteration (AD; 2 weeks). Based on individual ethanol intake, the mice were classified into three groups: A group, preference for ethanol and persistently high consumption during AD phase; B group, preference for ethanol and a reduction of ethanol intake in the AD phase; and C group; preference for water during all phases. A control group only had access to water. CRF1 receptor messenger RNA (mRNA) levels in the amygdala and the effect of the CRF1 receptor antagonist CP-154,526 on ethanol and water intake in the subgroups were studied.
resultsCRF1 transcript levels were higher in the B group than in the control group. The highest dose of CP-154,526 reduced ethanol intake and preference, with no changes in water consumption, in the A group compared with vehicle. The B group exhibited a reduction of both ethanol and water intake, with no changes in preference. The C group exhibited no changes in response to the CRF1 antagonist.
conclusionsCRF1 receptors appear to be involved in ethanol consumption in mice with high ethanol consumption, and CRF system-mediated neuroadaptations depend on drinking profiles.
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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.