Evidence map›Paper›PMID 31697943›Full record

ArticleExperimental neurology2020

Gastric vagal afferent neuropathy following experimental spinal cord injury.

Emily M Besecker, Emily N Blanke, Gina M Deiter, Gregory M Holmes

Open access · greenAbstract read
In one paragraph

Article in Experimental neurology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.9field-weighted citation impact, top 31% 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

14 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
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  4. Review
  5. Role of voltage-gated CaJournal of neurophysiology · 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

4 authors at 1 institution in 1 country.

Emily M BeseckerDepartment of Neural and Behavioral Sciences, Penn State University College of Medicine, Hershey, PA 17033, United States of America; Department of Health Sciences, Gettysburg College, Gettysburg, PA 17325, United States of America.
Emily N BlankeDepartment of Neural and Behavioral Sciences, Penn State University College of Medicine, Hershey, PA 17033, United States of America.
Gina M DeiterDepartment of Neural and Behavioral Sciences, Penn State University College of Medicine, Hershey, PA 17033, United States of America.
Gregory M HolmesDepartment of Neural and Behavioral Sciences, Penn State University College of Medicine, Hershey, PA 17033, United States of America. Electronic address: gmh16@psu.edu.
Pennsylvania State University · US

Funding

Gastric dysreflexia after spinal cord injuryR01NS049177 · NINDS · PENNSYLVANIA STATE UNIV HERSHEY MED CTR · PI HOLMES, GREGORY M. · 2006 to 2015
$3.1M
The role of TRPV1 in gastric dysmotility of the spinal cord injured rodent modelF31NS087834 · NINDS · PENNSYLVANIA STATE UNIV HERSHEY MED CTR · PI SWARTZ, EMILY MAE · 2014 to 2014
$13k
NINDS NIH HHS F31 NS087834NINDS NIH HHS R01 NS049177
6 · The paper itself

Abstract

Dramatic impairment of gastrointestinal (GI) function accompanies high-thoracic spinal cord injury (T3-SCI). The vagus nerve contains mechano- and chemosensory fibers as well as the motor fibers necessary for the central nervous system (CNS) control of GI reflexes. Cell bodies for the vagal afferent fibers are located within the nodose gangla (NG) and the majority of vagal afferent axons are unmyelinated C fibers that are sensitive to capsaicin through activation of transient receptor potential vanilloid-1 (TRPV1) channels. Vagal afferent fibers also express receptors for GI hormones, including cholecystokinin (CCK). Previously, T3-SCI provokes a transient GI inflammatory response as well as a reduction of both gastric emptying and centrally-mediated vagal responses to GI peptides, including CCK. TRPV1 channels and CCK-A receptors (CCKar) expressed in vagal afferents are upregulated in models of visceral inflammation. The present study investigated whether T3-SCI attenuates peripheral vagal afferent sensitivity through plasticity of TRPV1 and CCK receptors. Vagal afferent response to graded mechanical stimulation of the stomach was significantly attenuated by T3-SCI at 3-day and 3-week recovery. Immunocytochemical labeling for CCKar and TRPV1 demonstrated expression on dissociated gastric-projecting NG neurons. Quantitative assessment of mRNA expression by qRT-PCR revealed significant elevation of CCKar and TRPV1 in the whole NG following T3-SCI in 3-day recovery, but levels returned to normal after 3-weeks. Three days after injury, systemic administration of CCK-8 s showed a significantly diminished gastric vagal afferent response in T3-SCI rats compared to control rats while systemic capsaicin infusion revealed a significant elevation of vagal response in T3-SCI vs control rats. These findings demonstrate that T3-SCI provokes peripheral remodeling and prolonged alterations in the response of vagal afferent fibers to the physiological signals associated with digestion.

Indexed as

AnimalsAutonomic Nervous System DiseasesGastrointestinal MotilityMaleNeuronal PlasticityNeurons, AfferentRatsRats, WistarReceptors, CholecystokininSpinal Cord InjuriesStomachThoracic VertebraeTRPV Cation ChannelsVagus NerveReceptors, CholecystokininTRPV1 receptorTRPV Cation ChannelsCapsaicinCCK-1 receptorCCK-A receptorCholecystokininGastric emptyingGastrointestinal motilityNeurotraumaStomachTRPV1Vago-vagal reflexes

Identifiers

PMID31697943
PMCPMC6938028
OpenAlexW2982996425

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.