ArticleFrontiers in pharmacology2025
Reducing stress and alcohol-related behaviors by targeting D1-CRHR1 receptor interactions in the amygdala.
Article in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- The central amygdala corticotropin releasing factor system regulates anxiety-like behavior in an age- and sex- dependent manner in rats.Addiction neuroscience · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Basic neuroscience has identified dopamine and corticotropin-releasing hormone (CRH) systems and amygdala circuits as key contributors to drug and alcohol reward, craving, and relapse. However, directly targeting these systems has had no impact on the treatment of addictive disorders. CRH receptor 1 (CRHR1) and dopamine receptor D1 are both modulators of amygdala function. The intercalating cell masses (ITC) regulate intra-amygdala signal flow and are highly enriched in CRHR1 and D1. To date, interactions between these systems have not been extensively examined. We tested these interactions using a combination of Methods: The impact of CRHR1 activation on D1 was demonstrated using i. c.v. injection of either CRH (2 μg/μL) or stressin I (4 μg/2 μL) in naïve rats followed by D1 receptor autoradiography. We then injected stressin I (0.01 μg/0.5 μL) and stressin I in combination with the D1 antagonist SCH23390 (120 ng/0.5 μL) site-specifically into the ITC and tested animals in the Elevated-Plus-Maze (EPM), followed by saturated D1 receptor autoradiography. Alcohol dependence was also induced in rats and D1 Results: Pharmacological activation of CRHR1 by i. c.v. injection of CRH or stressin I increased D1 binding sites exclusively in the amygdala, but not in extra-amygdala brain regions. Site-specific CRHR1 activation in the amygdala/ITC was associated with increased anxiety-like behavior that was prevented by co-treatment with SCH23390. In dependent D1 Conclusion: Our findings suggest D1-CRHR1 interactions within the ITC of the amygdala in response to stress, alcohol behavior, and the development of dependence, thereby providing a novel mechanism that may be targetable by therapeutic polypharmacological interference.
Indexed as
Identifiers
What OpenQuestion holds
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.