Evidence map›Paper›PMID 30747446›Full record

ArticleThe Journal of physiology2019

Hyperexcitability and plasticity induced by sustained hypoxia on rectus abdominis motoneurons.

Melina P da Silva, Davi José A Moraes, Leni G H Bonagamba, André de Souza Mecawi, Wamberto A Varanda, Benedito H Machado

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
1.2field-weighted citation impact, top 24% 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

2 citing papers in PubMed, 14 citations in OpenAlex.

  1. Review
  2. Reflex of the Gracilis in Brain Death.Diagnostics (Basel, Switzerland) · 2022
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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

6 authors at 2 institutions in 1 country.

Melina P da SilvaSchool of Medicine of Ribeirão Preto, Department of Physiology, University of São Paulo, Ribeirão Preto, SP, Brazil.ORCID 0000-0001-5730-0993
Davi José A MoraesSchool of Medicine of Ribeirão Preto, Department of Physiology, University of São Paulo, Ribeirão Preto, SP, Brazil.ORCID 0000-0001-6132-0217
Leni G H BonagambaSchool of Medicine of Ribeirão Preto, Department of Physiology, University of São Paulo, Ribeirão Preto, SP, Brazil.
André de Souza MecawiPaulista School of Medicine, Department of Biophysics, Federal University of São Paulo, São Paulo, Brazil.ORCID 0000-0003-4517-6221
Wamberto A VarandaSchool of Medicine of Ribeirão Preto, Department of Physiology, University of São Paulo, Ribeirão Preto, SP, Brazil.
Benedito H MachadoSchool of Medicine of Ribeirão Preto, Department of Physiology, University of São Paulo, Ribeirão Preto, SP, Brazil.ORCID 0000-0001-5648-0929
Universidade de São Paulo · BRUniversidade Federal de São Paulo · BR

Funding

Fundação de Amparo à Pesquisa do Estado de São Paulo 2013/06077-5Fundação de Amparo à Pesquisa do Estado de São Paulo 2013/10484-5Fundação de Amparo à Pesquisa do Estado de São Paulo 2015/01073-3
6 · The paper itself

Abstract

key pointsAcute hypoxia induces active expiration in rectus abdominis (RA) muscles in conscious freely moving rats, although its overall contribution is smaller than in internal oblique (IO) muscles. Tonically active and silent RA motoneurons were identified in in vitro preparations of rat spinal cords. Sustained hypoxia (SH) increased the synaptic strength and induced morphological changes in tonically active RA motoneurons. Expiratory RA motoneurons were recorded in the in situ preparation and SH enhanced both the excitability and the synaptic transmission in those firing during the stage 2 expiration. The present study contributes to a better understanding of the mechanisms involved in SH recruitment of RA motoneurons to induce active expiration in rats. ABSTRACT: Rectus abdominis (RA) motoneurons translate the complex respiratory brainstem inputs into effective muscle contractions. Despite their fundamental role in respiration, their functional and morphological properties are not fully understood. In the present study, we investigated for the first time the contribution of RA muscle to active expiration and characterized RA motoneurons regarding their electrical, molecular and morphological profiles in control rats and in rats submitted to sustained hypoxia (SH), which induces chronic recruitment of abdominal muscles. Electromyographic experiments in conscious freely moving control rats and SH rats showed that RA contributes to active expiration induced by acute hypoxia, although its contribution is smaller than in internal oblique muscles. in vitro whole-cell patch clamp recordings from RA motoneurons revealed two populations of cells: tonically active and silent. SH induced hyperexcitability in the tonically active cells by changing their action potential properties, and EPSCs. Three-dimensional morphological reconstructions of these cells showed that SH increased the dendritic complexity, stimulated the appearance of dendrite spines, and increased the somatic area and volume. Physiologically identified RA motoneurons, firing in two distinct phases of expiration, were recorded in the brainstem-spinal cord in situ preparation of rats. SH increased the firing frequency and EPSCs of neurons firing during stage 2 expiration. Taken together, our results show that RA motoneurons reconfigure their biophysical properties, morphology and synaptic strength to produce an appropriate expiratory drive in response to SH in rats.

Indexed as

AnimalsBrain StemElectrophysiological PhenomenaMaleMotor NeuronsMuscle, SkeletalOxygenPatch-Clamp TechniquesRatsRats, WistarRespiratory Physiological PhenomenaSpinal CordOxygenactive ExpirationelectrophysiologyHypoxiaRectus abdominisSpinal motoneurons

Identifiers

PMID30747446
PMCPMC6441898
OpenAlexW2922334822

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.