ArticleThe Journal of physiology2004
Functional bradykinin B1 receptors are expressed in nociceptive neurones and are upregulated by the neurotrophin GDNF.
Article in The Journal of physiology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 98 citations in OpenAlex.
- Bradykinin receptor expression and bradykinin-mediated sensitization of human sensory neurons.bioRxiv : the preprint server for biology · 2023Article
- Global analyses of mRNA expression in human sensory neurons reveal eIF5A as a conserved target for inflammatory pain.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022Article
- SARS-CoV-2 involvement in central nervous system tissue damage.Neural regeneration research · 2022Review
- The des-ArgFrontiers in physiology · 2022Article
- Developmental defects and behavioral changes in a diet-induced inflammation model of zebrafish.Frontiers in immunology · 2022Article
- CR4056, a powerful analgesic imidazoline-2 receptor ligand, inhibits the inflammation-induced PKCε phosphorylation and membrane translocation in sensory neurons.British journal of pharmacology · 2020Article
- Beyond Trophic Factors: Exploiting the Intrinsic Regenerative Properties of Adult Neurons.Frontiers in cellular neuroscience · 2019Review
- Sympatho-excitatory response to pulmonary chemosensitive spinal afferent activation in anesthetized, vagotomized rats.Physiological reports · 2018Article
- Depolarizing Effectors of Bradykinin Signaling in Nociceptor Excitation in Pain Perception.Biomolecules & therapeutics · 2018Review
- Involvement of TRPV1 in the expression and release of calcitonin gene-related peptide induced by rutaecarpine.Molecular medicine reports · 2018Article
- New Insights into the Potential Roles of 3-Iodothyronamine (T1AM) and Newly Developed Thyronamine-Like TAAR1 Agonists in Neuroprotection.Frontiers in pharmacology · 2017Article
- Gabapentin Inhibits Protein Kinase C Epsilon Translocation in Cultured Sensory Neurons with Additive Effects When Coapplied with Paracetamol (Acetaminophen).TheScientificWorldJournal · 2017Article
- Modulatory and plastic effects of kinins on spinal cord networks.The Journal of physiology · 2016Article
- Bradykinin Induces TRPV1 Exocytotic Recruitment in Peptidergic Nociceptors.Frontiers in pharmacology · 2016Article
- The Cancer Chemotherapeutic Paclitaxel Increases Human and Rodent Sensory Neuron Responses to TRPV1 by Activation of TLR4.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- 3-iodothyroacetic acid, a metabolite of thyroid hormone, induces itch and reduces threshold to noxious and to painful heat stimuli in mice.British journal of pharmacology · 2015Article
- [1 + 1 = 0. Reprogramming of nociceptors].Schmerz (Berlin, Germany) · 2014Article
- Role for monocyte chemoattractant protein-1 in the induction of chronic muscle pain in the rat.Pain · 2014Article
- Characterisation of cannabinoid 1 receptor expression in the perikarya, and peripheral and spinal processes of primary sensory neurons.Brain structure & function · 2013Article
- Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
Bradykinin (BK) has long been recognized as an important mediator of pain and inflammation. In normal tissue bradykinin causes an acute sensation of pain by an action at B2 receptors, but in inflamed tissue the pharmacology of the response changes to that of B1 receptors. Attempts to demonstrate the presence of functional B1 receptors in sensory neurones have failed, however, and the actions of B1 agonists have therefore been presumed to be indirect. Here we show that specific B1 receptor activation causes translocation of the epsilon isoform of protein kinase C (PKC-epsilon) to the membrane of a small fraction of freshly isolated sensory neurones from rats and mice. The proportion of neurones in which PKC-epsilon translocation was observed increased to around 20% of neurones after 3 days in culture with the neurotrophins glial cell line derived neurotrophic factor (GDNF) and neurturin, but not with nerve growth factor (NGF). Using in situ hybridization we found that the proportion of neurones expressing B1 mRNA increased from close to zero to 20.4% after 8 h culture in GDNF. Neurones expressing functional B1 receptors were negative for the neuropeptides CGRP and substance P, but most expressed functional TRPV1 receptors for capsaicin (60%) and bound the lectin IB4 (68%), both markers characteristic of nociceptors. B1 activation enhanced the heat-activated membrane current approximately 3-fold, and the enhancement was much more prolonged than was the case with B2 activation, consistent with a role for B1 receptors in sustained pain. We conclude that GDNF and neurturin potently upregulate functional B1 receptor expression in small non-peptidergic nociceptive neurones.
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Registered trials
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