ArticleNeuropharmacology2025
Kappa opioid receptors diminish spontaneous dopamine signals in awake mice through multiple mechanisms.
Article in Neuropharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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
5 citing papers in PubMed.
- Dissecting the contribution of mu and kappa opioid receptor signalling in effort and delay-related cost/benefit decision making.Psychopharmacology · 2026Article
- Review
- From Monoamines to Systems Psychiatry: Rewiring Depression Science and Care (1960s-2025).Biomedicines · 2025Article
- Kappa opioid receptor antagonism restores phosphorylation, trafficking and behavior induced by a disease-associated dopamine transporter variant.Molecular psychiatry · 2025Article
- Fiber Photometry Analysis of Spontaneous Dopamine Signals: TheACS chemical neuroscience · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
The role of the dynorphin/kappa opioid receptor (KOR) system in dopamine (DA) regulation has been extensively investigated. KOR activation reduces extracellular DA concentrations, but the exact mechanism(s) through which this is accomplished are not fully elucidated. To explore KOR influences on real-time DA fluctuations, we used the photosensor dLight1.2 with fiber photometry in the nucleus accumbens (NAc) core of freely moving male and female C57BL/6J mice. First, we established that the rise and fall of spontaneously arising DA signals were due to DA release and reuptake, respectively. Next, mice were systemically administered the KOR agonist U50,488H in the presence or absence of the KOR antagonist aticaprant. U50,488H reduced both the amplitude and width of spontaneous signals in both sexes. Further, the slope of the correlation between amplitude and width was increased, indicating that DA uptake rates were increased. U50,488H also reduced the frequency of occurrence of signals in males and females. The effects of KOR activation were stronger in males, while effects of KOR antagonism were stronger in females. Overall, KORs exerted significant inhibitory control over spontaneous DA signaling, acting through at least three mechanisms - inhibiting DA release, promoting DA transporter-mediated uptake, and reducing the frequency of signals.
Indexed as
Identifiers
What Socratic 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 Socratic graph.