Evidence map›Paper›PMID 18456414›Full record

ArticleNeuroscience2008

Capsaicin-induced neuronal death and proliferation of the primary sensory neurons located in the nodose ganglia of adult rats.

K Czaja, G A Burns, R C Ritter

Open access · greenAbstract read
In one paragraph

Article in Neuroscience, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

34 citing papers in PubMed, 74 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Identification of Sodium Transients Through NaFrontiers in cellular neuroscience · 2022
    Article
  7. Review
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  9. Review
  10. Article
  11. Acute and chronic changes in the control of breathing in a rat model of bronchopulmonary dysplasia.American journal of physiology. Lung cellular and molecular physiology · 2019
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Vagal neurocircuitry and its influence on gastric motility.Nature reviews. Gastroenterology & hepatology · 2016
    Review
  18. Article
  19. Article
  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

3 authors at 1 institution in 1 country.

K CzajaDepartment of Veterinary, Comparative Anatomy, Pharmacology, and Physiology, College of Veterinary Medicine, Washington State University, Pullman, WA 99163-6520, USA. czajak@vetmed.wsu.edu
G A Burns
R C Ritter
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 DK-52849NIDDK NIH HHS R01 DK052849NINDS NIH HHS NS-20561NINDS NIH HHS R01 NS020561
6 · The paper itself

Abstract

To evaluate the potential for neuronal replacement following destruction of vagal afferent neurons, we examined nodose ganglia following i.p. capsaicin treatment of adult rats. Rats received capsaicin or vehicle followed by a regimen of 5'-bromo-2'-deoxyuridine injections (BrdU) to reveal DNA replication. Nodose ganglia were harvested at various times post-treatment and processed for 4',6-diamidino-2-phenylindole (DAPI) nuclear staining and immunofluorescence to estimate neuronal numbers and to determine vanilloid receptor, cleaved caspase 3, TUNEL, BrdU, the neuron-selective marker protein gene product (PGP) -9.5 and neurofilament-M-immunoreactivity. Twenty-four hours after capsaicin approximately 40% of nodose ganglion neurons expressed cleaved caspase 3-immunoreactivity and 16% revealed TUNEL staining, indicating that primary sensory neurons are killed by the capsaicin treatment of adult rats. The occurrence of neuronal death was confirmed by counts of DAPI-stained neuronal nuclei, which revealed >or=50% reduction of nodose neuron number by 30 days post-capsaicin. However, by 60 days post-capsaicin, the total numbers of neuronal nuclei in nodose ganglia from capsaicin-treated rats were not different from controls, suggesting that new neurons had been added to the nodose ganglia. Neuronal proliferation was confirmed by significant BrdU incorporation in nuclei of nodose ganglion cells immunoreactive for the neuron-specific antigen PGP-9.5 revealed 30 and 60 days post-capsaicin. Collectively, these observations suggest that in adult rats massive scale neurogenesis occurs in nodose ganglia following capsaicin-induced neuronal destruction. The adult nodose ganglion, therefore, provides a novel system for studying neural plasticity and adult neurogenesis after peripheral injury of primary sensory neurons.

Indexed as

AnimalsAntimetabolitesBromodeoxyuridineCapsaicinCaspase 3Cell DeathCell ProliferationFluorescent DyesImmunohistochemistryIndolesIn Situ Nick-End LabelingMaleMicroscopy, ElectronNeuronal PlasticityNeurons, AfferentNodose GanglionAntimetabolitesBromodeoxyuridineCapsaicinCaspase 3DAPIFluorescent DyesIndolesTrpv1 protein, ratTRPV Cation ChannelsUbiquitin ThiolesteraseUCHL1 protein, rat

Identifiers

PMID18456414
PMCPMC2527584
OpenAlexW2081646330

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.