Evidence map›Paper›PMID 22342909›Full record

ArticleNeuroscience letters2012

Changes in microglial activation within the hindbrain, nodose ganglia, and the spinal cord following subdiaphragmatic vagotomy.

Z R Gallaher, V Ryu, T Herzog, R C Ritter, K Czaja

Abstract read
In one paragraph

Article in Neuroscience letters, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

29 citing papers in PubMed, 48 citations in OpenAlex.

  1. Article
  2. Review
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  7. Unilateral vagotomy alters astrocyte and microglial morphology in the nucleus tractus solitarii of the rat.American journal of physiology. Regulatory, integrative and comparative physiology · 2021
    Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
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  14. Article
  15. The metabolic role of vagal afferent innervation.Nature reviews. Gastroenterology & hepatology · 2018
    Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. 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 at 1 institution in 1 country.

Z R GallaherProgram in Neuroscience, Department of Veterinary and Comparative Anatomy, Pharmacology and Physiology, Washington State University, Pullman, WA 99164, USA.
V Ryu
T Herzog
R C Ritter
K Czaja
Washington State University · US

Funding

The Role of Glutamate in the Control of Food IntakeR01DK052849 · NIDDK · WASHINGTON STATE UNIVERSITY · PI APPLEYARD, SUZANNE M, RITTER, ROBERT C · 1998 to 2021
$6.3M
NEURAL SUBSTRATES OF PEPTIDE-INDUCED SATIETYR01NS020561 · NINDS · WASHINGTON STATE UNIVERSITY · PI RITTER, ROBERT C · 1985 to 2012
$3.6M
NIDDK NIH HHS DK052849NIDDK NIH HHS R01 DK052849NINDS NIH HHS NS020561NINDS NIH HHS R01 NS020561
6 · The paper itself

Abstract

Damage to peripheral nerve branches triggers activation of microglia in CNS areas containing motor neuron soma and primary afferent terminals of the damaged fibers. Furthermore, microglial activation occurs in areas containing the soma and terminals of spared nerve branches of a damaged nerve. Because the abdominal viscera are innervated by spinal afferents as well as vagal afferents and efferents, we speculated that spinal nerves might respond like spared nerve branches following damage to vagal fibers. Therefore, we tested the hypothesis that damage to the abdominal vagus would result in microglial activation in vagal structures-the nucleus of the solitary tract (NTS), dorsal motor nucleus of the vagus nerve (DMV), and nodose ganglia (NG)-as well as spinal cord (SC) segments that innervate the abdominal viscera. To test this hypothesis, rats underwent subdiaphragmatic vagotomy or sham surgery and were treated with saline or the microglial inhibitor, minocycline. Microglial activation was determined by quantifying changes in the intensity of fluorescent staining with a primary antibody against ionizing calcium adapter binding molecule 1 (Iba1). We found that subdiaphragmatic vagotomy significantly activated microglia in the NTS, DMV, and NG two weeks post-vagotomy. Microglial activation remained significantly increased in the NG and DMV for at least 42 days. Surprisingly, vagotomy significantly decreased microglial activation in the SC. Minocycline treatment attenuated microglial activation in all studied areas. Our results indicate that microglial activation in vagal structures following abdominal vagal damage is accompanied by suppression of microglial activation in associated areas of the spinal cord.

Indexed as

VagotomyAnimalsAnti-Bacterial AgentsCalcium-Binding ProteinsDiaphragmMacrophage ActivationMaleMicrofilament ProteinsMicrogliaMicroscopy, FluorescenceMinocyclineNodose GanglionRatsRats, Sprague-DawleyRhombencephalonSolitary NucleusAif1 protein, ratAnti-Bacterial AgentsCalcium-Binding ProteinsMicrofilament ProteinsMinocycline

Identifiers

PMID22342909
PMCPMC3302977
OpenAlexW1996781477

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.