ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2007
Neurokinin-1 receptor enhances TRPV1 activity in primary sensory neurons via PKCepsilon: a novel pathway for heat hyperalgesia.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 108 papers.
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Who cites it
108 citing papers in PubMed, 192 citations in OpenAlex.
- Topical Ocular TRPV1 Antagonist SAF312 (Libvatrep) Demonstrates Safety, Low Systemic Exposure, and No Anesthetic Effect in Healthy Participants.Translational vision science & technology · 2022Trial
- Transient receptor potential vanilloid type-1 (TRPV-1) channels contribute to cutaneous thermal hyperaemia in humans.The Journal of physiology · 2010Trial
- Intradermal administration of magnesium sulphate and magnesium chloride produces hypesthesia to mechanical but hyperalgesia to heat stimuli in humans.Journal of neuroinflammation · 2009Trial
- In Vitro Reconstruction of Axonal Heat Sensing with a Photothermal Nerve-on-a-Chip.Small (Weinheim an der Bergstrasse, Germany) · 2026Article
- A transient receptor potential vanilloid 1-dependent corneal-trigeminal neuroinflammatory circuit promotes corneal neuropathy.Experimental & molecular medicine · 2026Article
- Human Dorsal Root Ganglia Neuronal Cell Line to Study Nociceptive Signaling: A New Pipeline for Pain Therapy.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Intravesical substance P enhances bladder afferent nerve activity without the influence of the micturition reflex.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Cibotii Rhizoma extract protects rat dorsal root ganglion neurons against HBMC complementary medicine and therapies · 2025Article
- Neuronal activity-induced GLUT3 plasma translocation supports energy demands for memory acquisition.Communications biology · 2025Article
- Targeting TRPV1 channels in desensitized neural afferent pathways may help mitigate pain and lower urinary tract symptoms caused by prostatitis.Frontiers in pharmacology · 2025Article
- 2-Kidney-1-clip hypertension is not attenuated in mice lacking the transient receptor potential vanilloid type 1 (TRPV1) channel.Frontiers in physiology · 2025Article
- TRPM7 Mediates Neuropathic Pain by Activating mTOR Signaling in Astrocytes after Spinal Cord Injury in Rats.Molecular neurobiology · 2024Article
- Evaluation ofMolecules (Basel, Switzerland) · 2024Article
- Pathophysiological Roles of Ion Channels in Epidermal Cells, Immune Cells, and Sensory Neurons in Psoriasis.International journal of molecular sciences · 2024Review
- The dual role of TRPV1 in peripheral neuropathic pain: pain switches caused by its sensitization or desensitization.Frontiers in molecular neuroscience · 2024Review
- Enhancement sensitivity of TRPV1 in dorsal root ganglia via the SP-NK-1 pathway contributes to increased bladder organ sensitivity caused by prostatitis.Frontiers in neuroscience · 2024Article
- Photobiomodulation and vitamin B treatment alleviate both thermal and mechanical orofacial pain in rats.Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology · 2023Article
- Kinin BPharmaceuticals (Basel, Switzerland) · 2023Article
- Review
- Nociception in fruit fly larvae.Frontiers in pain research (Lausanne, Switzerland) · 2023Review
48 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
The neuropeptide substance P (SP) is expressed in unmyelinated primary sensory neurons and represents the best known "pain" neurotransmitter. It is generally believed that SP regulates pain transmission and sensitization by acting on neurokinin-1 receptor (NK-1), which is expressed in postsynaptic dorsal horn neurons. However, the expression and role of NK-1 in primary sensory neurons are not clearly characterized. Our data showed that NK-1 was expressed in both intact and dissociated dorsal root ganglion (DRG) neurons. In particular, NK-1 was mainly coexpressed with the capsaicin receptor TRPV1 (transient receptor potential vanilloid subtype 1), a critical receptor for the generation of heat hyperalgesia. NK-1 agonist [Sar(9), Met(O2)(11)]-substance P (Sar-SP) significantly potentiated capsaicin-induced currents and increase of [Ca2+]i in dissociated DRG neurons. NK-1 antagonist blocked not only the potentiation of TRPV1 currents but also heat hyperalgesia induced by intraplantar Sar-SP. NK-1 antagonist also inhibited capsaicin-induced spontaneous pain, and this inhibition was enhanced after inflammation. To analyze intracellular cross talking of NK-1 and TRPV1, we examined downstream signal pathways of G-protein-coupled NK-1 activation. Sar-SP-induced potentiation of TRPV1 was blocked by inhibition of G-protein, PLCbeta (phospholipase C-beta), or PKC but not by inhibition of PKA (protein kinase A). In particular, PKCepsilon inhibitor completely blocked both Sar-SP-induced TRPV1 potentiation and heat hyperalgesia. Sar-SP also induced membrane translocation of PKCepsilon in a portion of small DRG neurons. These results reveal a novel mechanism of NK-1 in primary sensory neurons via a possible autocrine and paracrine action of SP. Activation of NK-1 in these neurons induces heat hyperalgesia via PKCepsilon-mediated potentiation of TRPV1.
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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.