Evidence map›Paper›PMID 31596498›Full record

ArticleBritish journal of pharmacology2020

Opioids differentially modulate two synapses important for pain processing in the amygdala.

Sarah A Kissiwaa, Sahil D Patel, Bryony L Winters, Elena E Bagley

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in British journal of pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.0field-weighted citation impact, top 13% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

18 citing papers in PubMed, 21 citations in OpenAlex.

  1. Role of the Amygdala in the Complex Relationship Between Sleep and Anxiety.International journal of molecular sciences · 2026
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  14. Molecular Genetics of Kappa Opioids in Pain and Itch Sensations.Handbook of experimental pharmacology · 2022
    Review
  15. Brain circuits for pain and its treatment.Science translational medicine · 2021
    Review
  16. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

Sarah A KissiwaaDiscipline of Pharmacology and Charles Perkins Centre, The University of Sydney, Sydney, NSW, Australia.
Sahil D PatelDiscipline of Pharmacology and Charles Perkins Centre, The University of Sydney, Sydney, NSW, Australia.
Bryony L WintersPain Management Research Institute, Kolling Institute of Medical Research, The University of Sydney, Royal North Shore Hospital, St Leonards, NSW, Australia.
Elena E BagleyDiscipline of Pharmacology and Charles Perkins Centre, The University of Sydney, Sydney, NSW, Australia.ORCID 0000-0002-3167-0707
The University of Sydney · AURoyal North Shore Hospital · AU

Funding

Bishop FellowshipFunder is Australian Pain Society Funder is Bosch Institute Bishop Fellowship PhD scholarshipNational Health and Medical Research Council APP1047372National Health and Medical Research Council APP1077806Northcote Trust
6 · The paper itself

Abstract

background and purposePain is a subjective experience involving sensory discriminative and emotionally aversive components. Consistent with its role in pain processing and emotions, the amygdala modulates the aversive component of pain. The laterocapsular region of the central nucleus of the amygdala (CeLC) receives nociceptive information from the parabrachial nucleus (PB) and polymodal, including nociceptive, inputs from the basolateral nucleus of the amygdala (BLA). Opioids are strong analgesics and reduce both the sensory discriminative and the affective component of pain. However, it is unknown whether opioids regulate activity at the two nociceptive inputs to the amygdala. EXPERIMENTAL APPROACH: Using whole-cell electrophysiology, optogenetics, and immunohistochemistry, we investigated whether opioids inhibit the rat PB-CeLC and BLA-CeLC synapses. KEY

resultsOpioids inhibited glutamate release at the PB-CeLC and BLA-CeLC synapses. Opioid inhibition is via the μ-receptor at the PB-CeLC synapse, while at the BLA-CeLC synapse, inhibition is via μ-receptors in all neurons and via δ-receptors and κ-receptors in a subset of neurons. CONCLUSIONS AND IMPLICATIONS: Agonists of μ-receptors inhibited two of the synaptic inputs carrying nociceptive information into the laterocapsular amygdala. Therefore, μ-receptor agonists, such as morphine, will inhibit glutamate release from PB and BLA in the CeLC, and this could serve as a mechanism through which opioids reduce the affective component of pain and pain-induced associative learning. The lower than expected regulation of BLA synaptic outputs by δ-receptors does not support the proposal that opioid receptor subtypes segregate into subnuclei of brain regions.

Indexed as

AmygdalaAnalgesics, OpioidAnimalsGlutamic AcidMaleNeural InhibitionNociceptionNociceptive PainOptogeneticsPain PerceptionRats, Sprague-DawleyReceptors, Opioid, deltaReceptors, Opioid, kappaReceptors, Opioid, muSynapsesAnalgesics, OpioidGlutamic AcidReceptors, Opioid, deltaReceptors, Opioid, kappaReceptors, Opioid, mu

Identifiers

PMID31596498
PMCPMC6989950
OpenAlexW2979848972

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.