Evidence map›Paper›PMID 23324998›Full record

ArticleCellular and molecular neurobiology2013

Retinal cell death induced by TRPV1 activation involves NMDA signaling and upregulation of nitric oxide synthases.

Mauro Leonelli, Daniel O Martins, Luiz R G Britto

Open access · greenAbstract read
In one paragraph

Article in Cellular and molecular neurobiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

16 citing papers in PubMed, 36 citations in OpenAlex.

  1. Review
  2. The Variety of Mechanosensitive Ion Channels in Retinal Neurons.International journal of molecular sciences · 2024
    Review
  3. Article
  4. Therapeutic Potential of Cannabinoids in Glaucoma.Pharmaceuticals (Basel, Switzerland) · 2023
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  13. Short-term increases in transient receptor potential vanilloid-1 mediate stress-induced enhancement of neuronal excitation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014
    Article
  14. Review
  15. Article
  16. Absence of transient receptor potential vanilloid-1 accelerates stress-induced axonopathy in the optic projection.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014
    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 2 institutions in 2 countries.

Mauro LeonelliLaboratory of Cellular Neurobiology, Department of Physiology & Biophysics, Institute of Biomedical Sciences, University of São Paulo, Av. Prof. Lineu Prestes, 1524, São Paulo, SP, 05508-000, Brazil. mauroleonelli@yahoo.com.br
Daniel O Martins
Luiz R G Britto
Universidade de São Paulo · BRInstitute of Biomedical Science · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The activation of the transient receptor potential vanilloid type 1 channel (TRPV1) has been correlated with oxidative and nitrosative stress and cell death in the nervous system. Our previous results indicate that TRPV1 activation in the adult retina can lead to constitutive and inducible nitric oxide synthase-dependent protein nitration and apoptosis. In this report, we have investigated the potential effects of TRPV1 channel activation on nitric oxide synthase (NOS) expression and function, and the putative participation of ionotropic glutamate receptors in retinal TRPV1-induced protein nitration, lipid peroxidation, and DNA fragmentation. Intravitreal injections of the classical TRPV1 agonist capsaicin up-regulated the protein expression of the inducible and endothelial NOS isoforms. Using 4,5-diaminofluorescein diacetate for nitric oxide (NO) imaging, we found that capsaicin also increased the production of NO in retinal blood vessels. Processes and perikarya of TRPV1-expressing neurons in the inner nuclear layer of the retina were found in the vicinity of nNOS-positive neurons, but those two proteins did not colocalize. Retinal explants exposed to capsaicin presented high protein nitration, lipid peroxidation, and cell death, which were observed in the inner nuclear and plexiform layers and in ganglion cells. This effect was partially blocked by AP-5, a NMDA glutamate receptor antagonist, but not by CNQX, an AMPA/kainate receptor antagonist. These data support a potential role for TRPV1 channels in physiopathological retinal processes mediated by NO, which at least in part involve glutamate release.

Indexed as

Signal TransductionUp-RegulationAldehydesAnimalsCell DeathDNA FragmentationIon Channel GatingLipid PeroxidationMaleNitric Oxide SynthaseNitric Oxide Synthase Type INitric Oxide Synthase Type IINitric Oxide Synthase Type IIINitrosationN-MethylaspartateRats3-nitrotyrosine4-hydroxy-2-nonenalAldehydesNitric Oxide SynthaseNitric Oxide Synthase Type INitric Oxide Synthase Type IINitric Oxide Synthase Type IIIN-MethylaspartateReceptors, N-Methyl-D-AspartateTrpv1 protein, ratTRPV Cation ChannelsTyrosine

Identifiers

PMID23324998
PMCPMC11497882
OpenAlexW2025091255

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.