Evidence map›Paper›PMID 27077912›Full record

ArticlePloS one2016

Activation of Brainstem Pro-opiomelanocortin Neurons Produces Opioidergic Analgesia, Bradycardia and Bradypnoea.

Serena Cerritelli, Stefan Hirschberg, Rob Hill, Nina Balthasar, Anthony E Pickering

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.5field-weighted citation impact, top 12% 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

22 citing papers in PubMed, 41 citations in OpenAlex.

  1. Cardiac vagal motor neurons.Current opinion in neurobiology · 2025
    Review
  2. Endogenous opioids and the development of the mammalian respiratory control network.American journal of physiology. Lung cellular and molecular physiology · 2025
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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

5 authors at 2 institutions in 1 country.

Serena CerritelliSchool of Physiology, Pharmacology & Neuroscience, Biomedical Sciences Building, University of Bristol, Bristol, BS8 1TD, United Kingdom.ORCID http://orcid.org/0000-0001-9548-3145
Stefan HirschbergSchool of Physiology, Pharmacology & Neuroscience, Biomedical Sciences Building, University of Bristol, Bristol, BS8 1TD, United Kingdom.
Rob HillSchool of Physiology, Pharmacology & Neuroscience, Biomedical Sciences Building, University of Bristol, Bristol, BS8 1TD, United Kingdom.
Nina BalthasarSchool of Physiology, Pharmacology & Neuroscience, Biomedical Sciences Building, University of Bristol, Bristol, BS8 1TD, United Kingdom.
Anthony E PickeringSchool of Physiology, Pharmacology & Neuroscience, Biomedical Sciences Building, University of Bristol, Bristol, BS8 1TD, United Kingdom.
University of Bristol · GBUniversity Hospitals Bristol NHS Foundation Trust · GB

Funding

Medical Research CouncilWellcome Trust 088373Wellcome Trust gr088373
6 · The paper itself

Abstract

Opioids are widely used medicinally as analgesics and abused for hedonic effects, actions that are each complicated by substantial risks such as cardiorespiratory depression. These drugs mimic peptides such as β-endorphin, which has a key role in endogenous analgesia. The β-endorphin in the central nervous system originates from pro-opiomelanocortin (POMC) neurons in the arcuate nucleus and nucleus of the solitary tract (NTS). Relatively little is known about the NTSPOMC neurons but their position within the sensory nucleus of the vagus led us to test the hypothesis that they play a role in modulation of cardiorespiratory and nociceptive control. The NTSPOMC neurons were targeted using viral vectors in a POMC-Cre mouse line to express either opto-genetic (channelrhodopsin-2) or chemo-genetic (Pharmacologically Selective Actuator Modules). Opto-genetic activation of the NTSPOMC neurons in the working heart brainstem preparation (n = 21) evoked a reliable, titratable and time-locked respiratory inhibition (120% increase in inter-breath interval) with a bradycardia (125±26 beats per minute) and augmented respiratory sinus arrhythmia (58% increase). Chemo-genetic activation of NTSPOMC neurons in vivo was anti-nociceptive in the tail flick assay (latency increased by 126±65%, p<0.001; n = 8). All effects of NTSPOMC activation were blocked by systemic naloxone (opioid antagonist) but not by SHU9119 (melanocortin receptor antagonist). The NTSPOMC neurons were found to project to key brainstem structures involved in cardiorespiratory control (nucleus ambiguus and ventral respiratory group) and endogenous analgesia (periaqueductal gray and midline raphe). Thus the NTSPOMC neurons may be capable of tuning behaviour by an opioidergic modulation of nociceptive, respiratory and cardiac control.

Indexed as

AnalgesiaAnalgesics, OpioidAnimalsArcuate Nucleus of HypothalamusBradycardiaBrain StemChannelrhodopsinsFemaleMaleMelanocyte-Stimulating HormonesMice, TransgenicMicroscopy, ConfocalNaloxoneNarcotic AntagonistsNeuronsPro-OpiomelanocortinAnalgesics, OpioidChannelrhodopsinsMelanocyte-Stimulating HormonesNaloxoneNarcotic AntagonistsPro-OpiomelanocortinSHU 9119

Identifiers

PMID27077912
PMCPMC4831707
OpenAlexW2339389944

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.