Evidence map›Paper›PMID 20804520›Full record

ArticleNeurogastroenterology and motility2010

Plasticity of vagal brainstem circuits in the control of gastric function.

K N Browning, R A Travagli

Open access · greenAbstract read
In one paragraph

Article in Neurogastroenterology and motility, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
6.2field-weighted citation impact, top 4% 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

58 citing papers in PubMed, 81 citations in OpenAlex.

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  13. Autonomic control of energy balance and glucose homeostasis.Experimental & molecular medicine · 2022
    Review
  14. Brain-gut communication: vagovagal reflexes interconnect the two "brains".American journal of physiology. Gastrointestinal and liver physiology · 2021
    Review
  15. Review
  16. Article
  17. Article
  18. Observational
  19. Article
  20. Electroacupuncture at ST36 modulates gastric motilityWorld journal of gastroenterology · 2019
    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

2 authors at 2 institutions in 1 country.

K N BrowningDepartment of Neural and Behavioral Sciences, Penn State College of Medicine, Hershey, PA 17033, USA. knb13@psu.edu
R A Travagli
Penn State Milton S. Hershey Medical Center · USPennsylvania State University · US

Funding

BRAINSTEM CIRCUITS CONTROLLING GASTROINTESTINAL FUNCTIONR01DK055530 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI BROWNING, KIRSTEEN NAIRN · 1998 to 2020
$4.6M
The effects of glucose on central vagal brainstem circuitsR01DK078364 · NIDDK · PENNSYLVANIA STATE UNIV HERSHEY MED CTR · PI BROWNING, KIRSTEEN NAIRN · 2010 to 2014
$1.4M
NIDDK NIH HHS DK078364NIDDK NIH HHS DK55530NIDDK NIH HHS R01 DK055530
6 · The paper itself

Abstract

backgroundSensory information from the viscera, including the gastrointestinal (GI) tract, is transmitted through the afferent vagus via a glutamatergic synapse to neurons of the nucleus tractus solitarius (NTS), which integrate this sensory information to regulate autonomic functions and homeostasis. The integrated response is conveyed to, amongst other nuclei, the preganglionic neurons of the dorsal motor nucleus of the vagus (DMV) using mainly GABA, glutamate and catecholamines as neurotransmitters. Despite being modulated by almost all the neurotransmitters tested so far, the glutamatergic synapse between NTS and DMV does not appear to be tonically active in the control of gastric motility and tone. Conversely, tonic inhibitory GABAergic neurotransmission from the NTS to the DMV appears critical in setting gastric tone and motility, yet, under basal conditions, this synapse appears resistant to modulation. PURPOSE: Here, we review the available evidence suggesting that vagal efferent output to the GI tract is regulated, perhaps even controlled, in an 'on-demand' and efficient manner in response to ever-changing homeostatic conditions. The focus of this review is on the plasticity induced by variations in the levels of second messengers in the brainstem neurons that form vago-vagal reflex circuits. Emphasis is placed upon the modulation of GABAergic transmission to DMV neurons and the modulation of afferent input from the GI tract by neurohormones/neurotransmitters and macronutrients. Derangement of this 'on-demand' organization of brainstem vagal circuits may be one of the factors underlying the pathophysiological changes observed in functional dyspepsia or hyperglycemic gastroparesis.

Indexed as

AnimalsBrain StemCyclic AMPDyspepsiagamma-Aminobutyric AcidGastrointestinal TractHumansNeural PathwaysNeuronal PlasticityNeurons, AfferentSolitary NucleusStomachSynapsesVagus NerveCyclic AMPgamma-Aminobutyric Acid

Identifiers

PMID20804520
PMCPMC2970760
OpenAlexW1746390316

What OpenQuestion holds

Textmetadata
LicenceTDM
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.