Evidence map›Paper›PMID 18480286›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2008

Mechanisms of prolonged presynaptic Ca2+ signaling and glutamate release induced by TRPV1 activation in rat sensory neurons.

Yuliya V Medvedeva, Man-Su Kim, Yuriy M Usachev

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed
4.6field-weighted citation impact, top 5% 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

65 citing papers in PubMed, 139 citations in OpenAlex.

  1. Review
  2. Article
  3. Mitochondrial CaBiomolecules · 2026
    Review
  4. Activation of TRPA1 and TRPM3 triggers CaThe Journal of physiology · 2025
    Article
  5. Article
  6. Mitochondrial CaCell calcium · 2025
    Article
  7. Article
  8. Frontiers in neuroinformatics · 2024
    Article
  9. Review
  10. Article
  11. Mitochondrial calcium cycling in neuronal function and neurodegeneration.Frontiers in cell and developmental biology · 2023
    Review
  12. Calcium Signalling in Breast Cancer Associated Bone Pain.International journal of molecular sciences · 2022
    Review
  13. Immune-Triggered Forms of Plasticity Across Brain Regions.Frontiers in cellular neuroscience · 2022
    Review
  14. Potential Role of Yoga Intervention in the Management of Chronic Non-malignant Pain.Evidence-based complementary and alternative medicine : eCAM · 2022
    Review
  15. Review
  16. Article
  17. Article
  18. Distinct properties of CaCell calcium · 2021
    Article
  19. Regulation of Mitochondrial Function by Epac2 Contributes to Acute Inflammatory Hyperalgesia.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Article
  20. Review

5 more citing papers are in PubMed but not listed here.

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.

Yuliya V MedvedevaDepartment of Pharmacology, University of Iowa Carver College of Medicine, Iowa City, Iowa 52242, USA.
Man-Su Kim
Yuriy M Usachev
University of Iowa · US

Funding

Mitochondrial Calcium Cycling in Neuronal FunctionR01NS054614 · NINDS · UNIVERSITY OF IOWA · PI USACHEV, YURIY M · 2006 to 2010
$1.6M
NINDS NIH HHS NS054614NINDS NIH HHS R01 NS054614
6 · The paper itself

Abstract

Transient receptor potential vanilloid receptor 1 (TRPV1)-mediated release of neuroactive peptides and neurotransmitters from the peripheral and central terminals of primary sensory neurons can critically contribute to nociceptive processing at the periphery and in the CNS. However, the mechanisms that link TRPV1 activation with Ca2+ signaling at the release sites and neurosecretion are poorly understood. Here we demonstrate that a brief stimulation of the receptor using either capsaicin or the endogenous TRPV1 agonist N-arachidonoyl-dopamine induces a prolonged elevation of presynaptic [Ca2+](i) and a concomitant enhancement of glutamate release at sensory synapses. Initiation of this response required Ca2+ entry, primarily via TRPV1. The sustained phase of the response was independent of extracellular Ca2+ and was prevented by inhibitors of mitochondrial Ca2+ uptake and release mechanisms. Measurements using a mitochondria-targeted Ca2+ indicator, mtPericam, revealed that TRPV1 activation elicits a long-lasting Ca2+ elevation in presynaptic mitochondria. The concentration of TRPV1 agonist determined the duration of mitochondrial and cytosolic Ca2+ signals in presynaptic boutons and, consequently, the period of enhanced glutamate release and action potential firing by postsynaptic neurons. These data suggest that mitochondria control vanilloid-induced neurotransmission by translating the strength of presynaptic TRPV1 stimulation into duration of the postsynaptic response.

Indexed as

Action PotentialsAfferent PathwaysAnimalsAnimals, NewbornArachidonic AcidsCalciumCalcium SignalingCapsaicinCells, CulturedCoculture TechniquesDopamineGanglia, SpinalGlutamic AcidMitochondriaNeurons, AfferentNociceptorsArachidonic Acidsarachidonyl dopamineCalciumCapsaicinDopamineGlutamic AcidTrpv1 protein, ratTRPV Cation Channels

Identifiers

PMID18480286
PMCPMC2694046
OpenAlexW2044513817

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.