ArticleAlcohol (Fayetteville, N.Y.)2012
The relationship between naloxone-induced cortisol and mu opioid receptor availability in mesolimbic structures is disrupted in alcohol dependent subjects.
Article in Alcohol (Fayetteville, N.Y.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- An experimental study on the role of naloxone in facilitating alcohol metabolism in acute alcohol intoxication rats.Future science OA · 2026Article
- Molecular Imaging Studies of Alcohol Use Disorder.Current topics in behavioral neurosciences · 2025Review
- The Role of Mu-Opioids for Reward and Threat Processing in Humans: Bridging the Gap from Preclinical to Clinical Opioid Drug Studies.Current addiction reports · 2021Review
- A Survey of Molecular Imaging of Opioid Receptors.Molecules (Basel, Switzerland) · 2019Review
- Is There a Role for GPCR Agonist Radiotracers in PET Neuroimaging?Frontiers in molecular neuroscience · 2019Review
- Corticotropin releasing hormone and imaging, rethinking the stress axis.Nuclear medicine and biology · 2015Review
- The effects of morphine, naloxone, and κ opioid manipulation on endocrine functioning and social behavior in monogamous titi monkeys (Callicebus cupreus).Neuroscience · 2015Article
- Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
The mu opioid receptor system is altered in alcohol dependent (AD) subjects. Cortisol responses to opioid receptor antagonists are assumed to impart information about opioid receptor activity. In the present study we examined naloxone-induced cortisol responses in 18 healthy control (HC) and 25 recently detoxified AD subjects and then correlated the cortisol response with mu opioid receptor availability across 15 brain regions using positron emission tomography (PET) and the mu opioid receptor selective ligand [(11)C] Carfentanil (CFN). On average the AD subjects required twice the dose of naloxone to induce a peak cortisol response compared to the HC subjects. Using the rising slope of the cortisol curve (placebo to peak) as a metric we then went on to examine the relationship between cortisol responses to naloxone and [(11)C]CFN BP(ND). There were significant negative relationships between cortisol and [(11)C]CFN binding potential (BP(ND)) in multiple brain regions of HC subjects. However, cortisol responses did not correlate with [(11)C]CFN BP(ND) across any brain region in AD subjects. In summary, naloxone imparts information about individual differences in mu opioid receptor availability throughout the mesolimbic system in healthy individuals. However pathways governing the relationship between naloxone-induced cortisol and mu opioid receptor availability are disrupted during early abstinence in AD subjects.
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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.