Evidence map›Paper›PMID 26794594›Full record

ArticleNeuroscience2016

Inflammation and activity augment brain-derived neurotrophic factor peripheral release.

L Y Qiao, S Shen, M Liu, C Xia, J C Kay, Q L Zhang

Abstract read
In one paragraph

Article in Neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
0.8field-weighted citation impact, top 30% 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

18 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
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  4. Article
  5. Cells · 2024
    Article
  6. Neuroimmune interplay in kidney health and disease: Role of renal nerves.Autonomic neuroscience : basic & clinical · 2023
    Review
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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 1 institution in 1 country.

L Y QiaoDepartment of Physiology and Biophysics, Virginia Commonwealth University, School of Medicine, Richmond, VA, United States. Electronic address: liya.qiao@vcuhealth.org.
S ShenDepartment of Physiology and Biophysics, Virginia Commonwealth University, School of Medicine, Richmond, VA, United States.
M LiuDepartment of Physiology and Biophysics, Virginia Commonwealth University, School of Medicine, Richmond, VA, United States.
C XiaDepartment of Physiology and Biophysics, Virginia Commonwealth University, School of Medicine, Richmond, VA, United States.
J C KayDepartment of Physiology and Biophysics, Virginia Commonwealth University, School of Medicine, Richmond, VA, United States.
Q L ZhangDepartment of Physiology and Biophysics, Virginia Commonwealth University, School of Medicine, Richmond, VA, United States.
Virginia Commonwealth University · US

Funding

Neurotrophins and Neuropeptides in Colon and Bladder HypersensitivityR01DK077917 · NIDDK · VIRGINIA COMMONWEALTH UNIVERSITY · PI QIAO, LIYA · 2008 to 2016
$2.8M
NIDDK NIH HHS R01 DK077917PHS HHS NIHDK077917
6 · The paper itself

Abstract

Brain-derived neurotrophic factor (BDNF) release to nerve terminals in the central nervous system is crucial in synaptic transmission and neuronal plasticity. However, BDNF release peripherally from primary afferent neurons has not been investigated. In the present study, we show that BDNF is synthesized by primary afferent neurons located in the dorsal root ganglia (DRG) in rat, and releases to spinal nerve terminals in response to depolarization or visceral inflammation. In two-compartmented culture that separates DRG neuronal cell bodies and spinal nerve terminals, application of 50mM K(+) to either the nerve terminal or the cell body evokes BDNF release to the terminal compartment. Inflammatory stimulation of the visceral organ (e.g. the urinary bladder) also facilitates an increase in spontaneous BDNF release from the primary afferent neurons to the axonal terminals. In the inflamed viscera, we show that BDNF immunoreactivity is increased in nerve fibers that are immuno-positive to the neuronal marker PGP9.5. Both BDNF and pro-BDNF levels are increased, however, pro-BDNF immunoreactivity is not expressed in PGP9.5-positive nerve-fiber-like structures. Determination of receptor profiles in the inflamed bladder demonstrates that BDNF high affinity receptor TrkB and general receptor p75 expression levels are elevated, with an increased level of TrkB tyrosine phosphorylation/activity. These results suggest a possibility of pro-proliferative effect in the inflamed bladder. Consistently we show that the proliferation marker Ki67 expression levels are enhanced in the inflamed organ. Our results imply that in vivo BDNF release to the peripheral organ is an important event in neurogenic inflammatory state.

Indexed as

AnimalsBrain-Derived Neurotrophic FactorGanglia, SpinalInflammationMaleNeurons, AfferentProtein PrecursorsRats, Sprague-DawleyReceptor, trkBSpinal CordBrain-Derived Neurotrophic Factorbrain-derived neurotrophic factor precursorProtein PrecursorsReceptor, trkBBDNFinflammationperipheryreceptorrelease

Identifiers

PMID26794594
PMCPMC4753152
OpenAlexW2273475235

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.