ArticleThe Journal of physiology2003
Signalling pathways involved in the sensitisation of mouse nociceptive neurones by nerve growth factor.
Article in The Journal of physiology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 139 papers.
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.
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.
Who cites it
139 citing papers in PubMed, 332 citations in OpenAlex.
- Targeting CXCR2 in Nociceptive Sensory Neurons Offers Novel Therapeutic Potentials for Postoperative Pain.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Chemokine CCL2 Mediates Neuroglial Crosstalk and Drives Chronic Pain Pathogenesis.Neuroscience bulletin · 2025Review
- IL-17 Stimulates Sensory Neurons and Sensitises Colonic Afferents to Noxious Stimuli in a PI3K Dependent Manner in Male Mice.Journal of neurochemistry · 2025Article
- Targeting NGF but not VEGFR1 or BDNF signaling reduces endometriosis-associated pain in mice.Journal of advanced research · 2025Article
- Pain research in a petri dish? Advantages and limitations of neuro-glial primary cell cultures from structures of the nociceptive system.Brain, behavior, & immunity - health · 2024Article
- Article
- Positive Allosteric Modulators of Trk Receptors for the Treatment of Alzheimer's Disease.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Light-Inducible Activation of TrkA for Probing Chronic Pain in Mice.ACS chemical biology · 2024Article
- Genetic code expansion, click chemistry, and light-activated PI3K reveal details of membrane protein trafficking downstream of receptor tyrosine kinases.bioRxiv : the preprint server for biology · 2024Article
- NGF Signaling Exacerbates KOA Peripheral Hyperalgesia via the Increased TRPV1-Labeled Synovial Sensory Innervation in KOA Rats.Pain research & management · 2024Article
- Predicting 'pain genes': multi-modal data integration using probabilistic classifiers and interaction networks.Bioinformatics advances · 2024Article
- Peripheral Neuroinflammation and Pain: How Acute Pain Becomes Chronic.Current neuropharmacology · 2024Review
- Bipartite Activation of Sensory Neurons by a TRPA1 Agonist Allyl Isothiocyanate Is Reflected by Complex CaInternational journal of molecular sciences · 2023Article
- Human Stem Cell-Derived TRPV1-Positive Sensory Neurons: A New Tool to Study Mechanisms of Sensitization.Cells · 2022Article
- Age-related changes in peripheral nociceptor function.Neuropharmacology · 2022Article
- Generation of Human Nociceptor-Enriched Sensory Neurons for the Study of Pain-Related Dysfunctions.Stem cells translational medicine · 2022Article
- Sensory TRP Channels in Three Dimensions.Annual review of biochemistry · 2022Review
- Molecular Effects of Low-Intensity Shock Wave Therapy on L6 Dorsal Root Ganglion/Spinal Cord and Blood Oxygenation Level-Dependent (BOLD) Functional Magnetic Resonance Imaging (fMRI) Changes in Capsaicin-Induced Prostatitis Rat Models.International journal of molecular sciences · 2022Article
- NGF Enhances CGRP Release Evoked by Capsaicin from Rat Trigeminal Neurons: Differential Inhibition by SNAP-25-Cleaving Proteases.International journal of molecular sciences · 2022Article
- Bradykinin-Induced Sensitization of Transient Receptor Potential Channel Melastatin 3 Calcium Responses in Mouse Nociceptive Neurons.Frontiers in cellular neuroscience · 2022Article
79 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nerve growth factor (NGF) causes a rapid sensitisation of nociceptive sensory neurones to painful thermal stimuli owing to an action on the heat and capsaicin receptor TRPV1 (formerly known as VR1). We have developed a new technique to study this rapid sensitisation of TRPV1 by monitoring the effects of NGF on the increase in intracellular calcium concentration ([Ca2+]i) following exposure to capsaicin. Brief applications of capsaicin caused a rise in [Ca2+]i, and NGF was found to enhance this rise in 37 % of capsaicin-responsive neurones within 2 min. Pathways responsible for transducing the sensitisation of TRPV1 by TrkA, the NGF receptor, were characterised by observing the effects of inhibitors of key members of NGF-activated second messenger signalling cascades. Specific inhibitors of the ras/MEK (mitogen-activated protein and extracellular signal-regulated kinases) pathway and of phospholipase C did not abolish the NGF-induced sensitisation, but wortmannin, a specific inhibitor of phosphatidylinositol-3-kinase (PI3K), totally abolished the effect of NGF. Pharmacological blockade of protein kinase C (PKC) or calcium-calmodulin-dependent protein kinase II (CaMK II) activation also prevented NGF-induced sensitisation, while blockade of protein kinase A (PKA) was without effect. These data indicate that the crucial early pathway activated by NGF involves PI3K, while PKC and CaMK II are also involved, probably at subsequent stages of the NGF-activated signalling pathway.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.