ArticleThe Journal of clinical investigation2010
Some new insights into the molecular mechanisms of pain perception.
Article in The Journal of clinical investigation, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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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.
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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.
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Who cites it
13 citing papers in PubMed, 27 citations in OpenAlex.
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- DAGLα Inhibition as a Non-invasive and Translational Model of Episodic Headache.Frontiers in pharmacology · 2020Article
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- Kv7 channels are upregulated during striatal neuron development and promote maturation of human iPSC-derived neurons.Pflugers Archiv : European journal of physiology · 2018Article
- Control of sensory neuron excitability by serotonin involves 5HT2C receptors and Ca(2+)-activated chloride channels.Neuropharmacology · 2016Article
- A Role for Bradykinin Signaling in Chronic Vulvar Pain.The journal of pain · 2016Article
- Inhibition of G protein-coupled P2Y2 receptor induced analgesia in a rat model of trigeminal neuropathic pain.Molecular pain · 2014Article
- The fundamental unit of pain is the cell.Pain · 2013Review
- TMEM16A alternative splicing coordination in breast cancer.Molecular cancer · 2013Article
- M channel enhancers and physiological M channel block.The Journal of physiology · 2012Article
- Anoctamins.Pflugers Archiv : European journal of physiology · 2011Review
- Article
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2 authors at 1 institution in 1 country.
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Abstract
Bradykinin is the most potent endogenous inducer of acute pain. However, the way in which it excites nociceptive sensory nerve endings is still unclear. In an article recently published in the JCI, Liu et al. suggest a new mechanism via which bradykinin induces acute spontaneous pain. The authors report that the stimulation of B2 bradykinin receptors by bradykinin triggers the release of intracellular calcium ions from nociceptive sensory neurons of rat dorsal root ganglia. This depolarizes the sensory nerve endings by simultaneously closing M-type potassium channels and opening TMEM16A chloride channels, resulting in the production of nociceptive signals. Here, we discuss the relationship between this effect and a previously described mechanism for pain sensitization and evaluate its potential significance for therapeutic pain control. A separate study by Patwardhan et al. in this issue of the JCI identifies oxidized linoleic acid metabolites as novel mediators of thermally induced pain.
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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.