ArticleAddiction biology2016
Dissociation of μ-opioid receptor and CRF-R1 antagonist effects on escalated ethanol consumption and mPFC serotonin in C57BL/6J mice.
Article in Addiction biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
21 citing papers in PubMed, 24 citations in OpenAlex.
- BLA kappa opioid receptor inputs to the BNST mediate social stress-induced increases in alcohol drinking.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026Article
- Functional remodeling of the parasubthalamic nucleus drives alcohol drinking escalation in dependence.bioRxiv : the preprint server for biology · 2026Article
- Modeling escalation of drug intake to identify molecular targets for treating substance use disorders: A slippery slope upward.Neuroscience and biobehavioral reviews · 2025Review
- Monoamine Transporters in Drugs of Abuse: Insights from Fast Scan Cyclic Voltammetry.Advances in neurobiology · 2025Review
- BLAbioRxiv : the preprint server for biology · 2024Article
- Mouse parasubthalamicbioRxiv : the preprint server for biology · 2024Article
- Serotonin regulation of intermittent and continuous alcohol drinking in male and female C57BL/6J mice with systemic SB242084 and buspirone.Alcohol and alcoholism (Oxford, Oxfordshire) · 2023Article
- Central amygdala corticotropin-releasing factor neurons promote hyponeophagia but do not control alcohol drinking in mice.Molecular psychiatry · 2022Article
- Friend of the Devil: Negative Social Influences Driving Substance Use Disorders.Frontiers in behavioral neuroscience · 2022Review
- Alterations in corticotropin-releasing factor receptor type 1 in the preoptic area and hypothalamus in mice during the postpartum period.Hormones and behavior · 2021Article
- Timing Eclipses Amount: The Critical Importance of Intermittency in Alcohol Exposure Effects.Alcoholism, clinical and experimental research · 2020Review
- Predator odor increases avoidance and glutamatergic synaptic transmission in the prelimbic cortex via corticotropin-releasing factor receptor 1 signaling.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2019Article
- CRF modulation of central monoaminergic function: Implications for sex differences in alcohol drinking and anxiety.Alcohol (Fayetteville, N.Y.) · 2018Review
- Social defeat stress and escalation of cocaine and alcohol consumption: Focus on CRF.Neurobiology of stress · 2018Review
- Persistent escalation of alcohol consumption by mice exposed to brief episodes of social defeat stress: suppression by CRF-R1 antagonism.Psychopharmacology · 2018Article
- CRF type 1 receptor antagonism in ventral tegmental area of adolescent rats during social defeat: prevention of escalated cocaine self-administration in adulthood and behavioral adaptations during adolescence.Psychopharmacology · 2016Article
- Serotonergic Neuroplasticity in Alcohol Addiction.Brain plasticity (Amsterdam, Netherlands) · 2016Review
- Social stress-escalated intermittent alcohol drinking: modulation by CRF-R1 in the ventral tegmental area and accumbal dopamine in mice.Psychopharmacology · 2016Article
- An Update on CRF Mechanisms Underlying Alcohol Use Disorders and Dependence.Frontiers in endocrinology · 2016Review
- Alcohol and violence: neuropeptidergic modulation of monoamine systems.Annals of the New York Academy of Sciences · 2015Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Both the opioid antagonist naltrexone and corticotropin-releasing factor type-1 receptor (CRF-R1) antagonists have been investigated for the treatment of alcoholism. The current study examines the combination of naltrexone and CP154526 to reduce intermittent access ethanol drinking [intermittent access to alcohol (IAA)] in C57BL/6J male mice, and if these compounds reduce drinking via serotonergic mechanisms in the dorsal raphe nucleus (DRN). Systemic injections and chronic intracerebroventricular infusions of naltrexone, CP154526 or CP376395 transiently decreased IAA drinking. Immunohistochemistry revealed CRF-R1 or μ-opioid receptor immunoreactivity was co-localized in tryptophan hydroxylase (TPH)-immunoreactive neurons as well as non-TPH neurons in the DRN. Mice with a history of IAA or continuous access to alcohol were microinjected with artificial cerebral spinal fluid, naltrexone, CP154526 or the combination into the DRN or the median raphe nucleus (MRN). Either intra-DRN naltrexone or CP154526 reduced IAA in the initial 2 hours of fluid access, but the combination did not additively suppress IAA, suggesting a common mechanism via which these two compounds affect intermittent drinking. These alcohol-reducing effects were localized to the DRN of IAA drinkers, as intra-MRN injections only significantly suppressed water drinking, and continuous access drinkers were not affected by CRF-R1 antagonism. Extracellular serotonin was measured in the medial prefrontal cortex (mPFC) using in vivo microdialysis after intra-DRN microinjections in another group of mice. Intra-DRN CP154526 increased serotonin impulse flow to the mPFC while naltrexone did not. This suggests the mPFC may not be an essential location to intermittent drinking, as evidenced by different effects on serotonin signaling to the forebrain yet similar behavioral findings.
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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.