Evidence map›Paper›PMID 31971507›Full record

ArticleeLife2020

C1 neurons are part of the circuitry that recruits active expiration in response to the activation of peripheral chemoreceptors.

Milene R Malheiros-Lima, Josiane N Silva, Felipe C Souza, Ana C Takakura, Thiago S Moreira

Abstract read
In one paragraph

Article in eLife, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
–field-weighted citation impact
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

17 citing papers in PubMed.

  1. Review
  2. Article
  3. Functional modulation of retrotrapezoid neurons drives fentanyl-induced respiratory depression.American journal of physiology. Lung cellular and molecular physiology · 2025
    Article
  4. Review
  5. Article
  6. Article
  7. Adrenergic C1 neurons enhance anxiety via projections to PAG.bioRxiv : the preprint server for biology · 2024
    Article
  8. Article
  9. eLife · 2022
    Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Differential Contribution of the Retrotrapezoid Nucleus and C1 Neurons to Active Expiration and Arousal in Rats.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
    Article
  17. Article
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.

Milene R Malheiros-LimaDepartment of Physiology and Biophysics, Institute of Biomedical Science, University of São Paulo, São Paulo, Brazil.
Josiane N SilvaDepartment of Pharmacology, Institute of Biomedical Science, University of São Paulo, São Paulo, Brazil.
Felipe C SouzaDepartment of Pharmacology, Institute of Biomedical Science, University of São Paulo, São Paulo, Brazil.
Ana C TakakuraDepartment of Pharmacology, Institute of Biomedical Science, University of São Paulo, São Paulo, Brazil.
Thiago S MoreiraDepartment of Physiology and Biophysics, Institute of Biomedical Science, University of São Paulo, São Paulo, Brazil.ORCID 0000-0002-9789-8296

Funding

Conselho Nacional de Desenvolvimento Científico e Tecnológico 301219/2016-8Conselho Nacional de Desenvolvimento Científico e Tecnológico 301904/2015-4Coordenação de Aperfeiçoamento de Pessoal de Nível Superior Finance Code 001Fundação de Amparo à Pesquisa do Estado de São Paulo 2015/23376-1Fundação de Amparo à Pesquisa do Estado de São Paulo 2016/23281-3Fundação de Amparo à Pesquisa do Estado de São Paulo Graduate Student Fellowship
6 · The paper itself

Abstract

Breathing results from the interaction of two distinct oscillators: the pre-Bötzinger Complex (preBötC), which drives inspiration; and the lateral parafacial region (pFRG), which drives active expiration. The pFRG is silent at rest and becomes rhythmically active during the stimulation of peripheral chemoreceptors, which also activates adrenergic C1 cells. We postulated that the C1 cells and the pFRG may constitute functionally distinct but interacting populations for controlling expiratory activity during hypoxia. We found in rats that: a) C1 neurons are activated by hypoxia and project to the pFRG region; b) active expiration elicited by hypoxia was blunted after blockade of ionotropic glutamatergic receptors at the level of the pFRG; and c) selective depletion of C1 neurons eliminated the active expiration elicited by hypoxia. These results suggest that C1 cells may regulate the respiratory cycle, including active expiration, under hypoxic conditions.

Indexed as

AnimalsCatecholaminesChemoreceptor CellsExcitatory Amino Acid AntagonistsExhalationGlutamatesHypoxiaKynurenic AcidMaleNeuronsRatsRats, WistarReceptors, AdrenergicReceptors, Ionotropic GlutamateRespirationCatecholaminesExcitatory Amino Acid AntagonistsGlutamatesKynurenic AcidReceptors, AdrenergicReceptors, Ionotropic Glutamatebreathingexpirationhypoxianeuroscienceoptogeneticsratventrolateral medulla

Identifiers

PMID31971507
PMCPMC7010411

What OpenQuestion holds

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LicenceCC BY
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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.