ArticleJournal of neurophysiology2025
Inhibitory effects of dopamine agonists on pain-responsive neurons in the central nucleus of the amygdala.
Article in Journal of neurophysiology, 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.
- Differential roles of dopamine D1 and D2 receptors in pain modulation: a review.Frontiers in neurologyReview
Corrections and comments
- Update of
Authors and funding
2 authors.
Funding
Abstract
The central nucleus of the amygdala (CeA) is a heterogeneous region of primarily GABAergic neurons that contribute to numerous behaviors, including fear learning, feeding, reward, and pain. Dopaminergic inputs to the CeA have been shown to regulate many of these behaviors, but how dopamine exerts these effects at the cellular level has not been well characterized. We used the targeted recombination in active populations (TRAP) mouse line to fluorescently label pain-responsive CeA neurons, and then targeted these cells for patch-clamp recordings in acute slices to test the effects of dopamine agonists. The D1 agonist SKF-38393 and D2 agonist quinpirole both had inhibitory effects, reducing the input resistance and evoked firing and increasing rheobase of labeled CeA neurons. Both agents also inhibited the NMDA component of excitatory postsynaptic currents (EPSCs) evoked by basolateral amygdala (BLA) stimulation, but did not affect the AMPA component. D1 activation, but not D2, also had a possible presynaptic effect, increasing the frequency of spontaneous EPSCs. These results provide new insights into how dopamine regulates activity within pain-responsive CeA networks.
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.