ArticleMolecular pain2009
PKCepsilon-dependent potentiation of TTX-resistant Nav1.8 current by neurokinin-1 receptor activation in rat dorsal root ganglion neurons.
Article in Molecular pain, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed.
- Sulfolipid-1 fromJournal of neurophysiology · 2026Article
- Upregulation of NaCells · 2022Article
- PKC regulation of ion channels: The involvement of PIPThe Journal of biological chemistry · 2022Review
- Growth Differentiation Factor-15 Produces Analgesia by Inhibiting Tetrodotoxin-Resistant Nav1.8 Sodium Channel Activity in Rat Primary Sensory Neurons.Neuroscience bulletin · 2021Article
- Pacific-Ciguatoxin-2 and Brevetoxin-1 Induce the Sensitization of Sensory Receptors Mediating Pain and Pruritus in Sensory Neurons.Marine drugs · 2021Article
- Neurogenic substance P-influences on action potential production in afferent neurons of the kidney?Pflugers Archiv : European journal of physiology · 2021Article
- Elevated Expression and Activity of Sodium Leak Channel Contributes to Neuronal Sensitization of Inflammatory Pain in Rats.Frontiers in molecular neuroscience · 2021Article
- Novel Analgesics with Peripheral Targets.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2020Review
- Repressor element 1-silencing transcription factor drives the development of chronic pain states.Pain · 2019Article
- Nociceptor Signalling through ion Channel Regulation via GPCRs.International journal of molecular sciences · 2019Review
- Ion Channels Involved in Substance P-Mediated Nociception and Antinociception.International journal of molecular sciences · 2019Review
- Endothelin type A receptors mediate pain in a mouse model of sickle cell disease.Haematologica · 2018Article
- Modulation of Nav1.8 by Lysophosphatidic Acid in the Induction of Bone Cancer Pain.Neuroscience bulletin · 2016Article
- Redox-Dependent Modulation of T-Type Ca(2+) Channels in Sensory Neurons Contributes to Acute Anti-Nociceptive Effect of Substance P.Antioxidants & redox signaling · 2016Article
- Epac-protein kinase C alpha signaling in purinergic P2X3R-mediated hyperalgesia after inflammation.Pain · 2016Article
- Phosphoinositide signaling in somatosensory neurons.Advances in biological regulation · 2016Review
- Serotonin Receptor 2B Mediates Mechanical Hyperalgesia by Regulating Transient Receptor Potential Vanilloid 1.Journal of molecular neuroscience : MN · 2016Article
- Dexmedetomidine inhibits Tetrodotoxin-resistant Nav1.8 sodium channel activity through Gi/o-dependent pathway in rat dorsal root ganglion neurons.Molecular brain · 2015Article
- Protein kinase Cδ mediates histamine-evoked itch and responses in pruriceptors.Molecular pain · 2015Article
- Post-translational modifications of voltage-gated sodium channels in chronic pain syndromes.Frontiers in pharmacology · 2015Review
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Authors and funding
4 authors.
Funding
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Abstract
backgroundSubstance P (SP), which mainly exists in a subtype of small-diameter dorsal root ganglion (DRG) neurons, is an important signal molecule in pain processing in the spinal cord. Our previous results have proved the expression of SP receptor neurokinin-1 (NK-1) on DRG neurons and its interaction with transient receptor potential vanilloid 1 (TRPV1) receptor.
resultsIn this study we investigated the effect of NK-1 receptor agonist on Na(v)1.8, a tetrodotoxin (TTX)-resistant sodium channel, in rat small-diameter DRG neurons employing whole-cell patch clamp recordings. NK-1 agonist [Sar(9), Met(O2)(11)]-substance P (Sar-SP) significantly enhanced the Na(v)1.8 currents in a subgroup of small-diameter DRG neurons under both the normal and inflammatory situation, and the enhancement was blocked by NK-1 antagonist Win51708 and protein kinase C (PKC) inhibitor bisindolylmaleimide (BIM), but not the protein kinase A (PKA) inhibitor H89. In particular, the inhibitor of PKCepsilon, a PKC isoform, completely blocked this effect. Under current clamp model, Sar-SP reduced the amount of current required to evoke action potentials and increased the firing rate in a subgroup of DRG neurons.
conclusionThese data suggest that activation of NK-1 receptor potentiates Na(v)1.8 sodium current via PKCepsilon-dependent signaling pathway, probably participating in the generation of inflammatory hyperalgesia.
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