ArticleAlcoholism, clinical and experimental research2013
CRF1 receptor signaling regulates food and fluid intake in the drinking-in-the-dark model of binge alcohol consumption.
Article in Alcoholism, clinical and experimental research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 57 citations in OpenAlex.
- A Distinct Subpopulation of Extended Amygdala Neurons Drives Food Intake.Biological psychiatry global open science · 2026Article
- Functional remodeling of the parasubthalamic nucleus drives alcohol drinking escalation in dependence.bioRxiv : the preprint server for biology · 2026Article
- A Distinct Subpopulation of Extended Amygdala Neurons Drives Food Intake.bioRxiv : the preprint server for biology · 2025Article
- Evidence for independent actions of the CRF and ghrelin systems in binge-like alcohol drinking in mice.Progress in neuro-psychopharmacology & biological psychiatry · 2025Article
- Traumatic stress-enhanced ethanol drinking: Sex, but not stress responsivity, alters sensitivity to the effects of a CRF-R1 antagonist and a GPR39 agonist in mice.Alcohol, clinical & experimental research · 2025Article
- Animal Models of Excessive Alcohol Consumption in Rodents.Current topics in behavioral neurosciences · 2025Review
- Stress-enhanced ethanol drinking does not increase sensitivity to the effects of a CRF-R1 antagonist on ethanol intake in male and female mice.Alcohol (Fayetteville, N.Y.) · 2024Article
- Behavioral and Amygdala Biochemical Damage Induced by Alternating Mild Stress and Ethanol Intoxication in Adolescent Rats: Reversal by Argan Oil Treatment?International journal of molecular sciences · 2024Article
- Mouse parasubthalamicbioRxiv : the preprint server for biology · 2024Article
- Neuroimmune interactions with binge alcohol drinking in the cerebellum of IL-6 transgenic mice.Neuropharmacology · 2023Article
- Central amygdala corticotropin-releasing factor neurons promote hyponeophagia but do not control alcohol drinking in mice.Molecular psychiatry · 2022Article
- Effect of early life social adversity on drug abuse vulnerability: Focus on corticotropin-releasing factor and oxytocin.Neuropharmacology · 2021Review
- Recent Perspectives on Sex Differences in Compulsion-Like and Binge Alcohol Drinking.International journal of molecular sciences · 2021Review
- Social Housing Leads to Increased Ethanol Intake in Male Mice Housed in Environmentally Enriched Cages.Frontiers in behavioral neuroscience · 2021Article
- Role of corticotropin-releasing factor in alcohol and nicotine addiction.Brain research · 2020Review
- Biological intersection of sex, age, and environment in the corticotropin releasing factor (CRF) system and alcohol.Neuropharmacology · 2020Review
- Biparental care in C57BL/6J mice: effects on adolescent behavior and alcohol consumption.Psychopharmacology · 2020Article
- Differential sensitivity of alcohol drinking and partner preference to a CRFR1 antagonist in prairie voles and mice.Hormones and behavior · 2020Article
- From Pleasure to Pain, and Back Again: The Intricate Relationship Between Alcohol and Nociception.Alcohol and alcoholism (Oxford, Oxfordshire) · 2019Review
- NOP Receptor Antagonists Decrease Alcohol Drinking in the Dark in C57BL/6J Mice.Alcoholism, clinical and experimental research · 2019Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
backgroundSeveral recent studies implementing the standard "drinking-in-the-dark" (DID) model of short-term binge-like ethanol (EtOH) intake in C57BL/6J mice highlighted a role for the stress-related neuropeptide corticotropin-releasing factor (CRF) and its primary binding partner, the CRF type-1 (CRF1) receptor.
methodsWe evaluated the selectivity of CRF1 involvement in binge-like EtOH intake by interrupting CRF1 function via pharmacological and genetic methods in a slightly modified 2-bottle choice DID model that allowed calculation of an EtOH preference ratio. In addition to determining EtOH intake and preference, we also measured consumption of food and H2 O during the DID period, both in the presence and absence of EtOH and sweet tastant solutions.
resultsTreatment with either of the CRF1-selective antagonists CP-376,395 (CP; 10 to 20 mg/kg, i.p.) or NBI-27914 (10 to 30 mg/kg, i.p.) decreased intake of 15% EtOH in male C57BL/6J mice, but did so in the absence of a concomitant decrease in EtOH preference. These findings were replicated genetically in a CRF1 knockout (KO) mouse model (also on a C57BL/6J background). In contrast to effects on EtOH intake, pharmacological blockade of CRF1 with CP increased intake of 10% sucrose, consistent with previous findings in CRF1 KO mice. Finally, pharmacological and genetic disruption of CRF1 activity significantly reduced feeding and/or total caloric intake in all experiments, confirming the existence of nonspecific effects.
conclusionsOur findings indicate that blockade of CRF1 receptors does not exert specific effects on EtOH intake in the DID paradigm, and that slight modifications to this procedure, as well as additional consummatory control experiments, may be useful when evaluating the selectivity of pharmacological and genetic manipulations on binge-like EtOH intake.
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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.