INT76660
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
The vanilloid receptor (TRPV1) is a member of the transient receptor potential family of ion channels that is highly expressed in nociceptive primary afferent sensory neurons. | |||||||||||||||
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The vanilloid receptor (TRPV1) is a member of the transient receptor potential family of ion channels that is highly expressed in nociceptive primary afferent sensory neurons. | |||||||||||||||
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The present review summarizes the properties of the TRPV1 ion channel known to be expressed in lung C-fibre afferents, the possible role of TRPV1 in respiratory sensation and neurogenic inflammation, as well as the limitations and opportunities associated with current TRPV1 antagonists. | |||||||||||||||
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Recent advances in pain biology such as the cloning of the transient receptor potential vanilloid 1 (TRPV1) ion channel, exploration of the molecular mechanisms leading to TRPV1 activation and the production of a TRPV1 mutant mouse have defined its role as an integrator of noxious thermal and chemical stimuli. | |||||||||||||||
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The capsaicin receptor TRPV1 (transient receptor potential vanilloid subtype 1) is a cation channel expressed by nociceptors that detects multiple pain-producing stimuli, including noxious heat and extracellular protons, raising the possibility that it is an important mediator of bone cancer pain via its capacity to detect osteoclast- and tumor-mediated tissue acidosis. | |||||||||||||||
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The transient receptor potential vanilloid 1 receptor (TRPV1) is expressed predominantly in a subset of primary afferent nociceptors. | |||||||||||||||
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The transient receptor potential vanilloid 1 receptor (TRPV1) is expressed predominantly in a subset of primary afferent nociceptors. | |||||||||||||||
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If so, it is conceivable that such TRPV1 ligands can be synthesized that specifically target TRPV1 in diseased (e.g. inflamed or neoplastic) tissues but spare TRPV1 that subserves its physiological functions in healthy organs. | |||||||||||||||
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Increased expression of vanilloid receptor 1 on myelinated primary afferent neurons contributes to the antihyperalgesic effect of capsaicin cream in diabetic neuropathic pain in mice. | |||||||||||||||
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Here, we report that an up-regulation of VR1 expression on myelinated fibers contributes to the antihyperalgesic effect of capsaicin cream in streptozotocin (STZ)-induced diabetic neuropathic pain. | |||||||||||||||
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Finally, we confirmed the up-regulation of VR1 expression on myelinated primary afferent neurons of diabetic mice by immunohistochemistry. | |||||||||||||||
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TRPV1, the capsaicin receptor, is expressed not only in nociceptive neurons, but also in other locations, including the hypothalamus. | |||||||||||||||
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TRPV1, the capsaicin receptor, is expressed not only in nociceptive neurons, but also in other locations, including the hypothalamus. | |||||||||||||||
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In the urinary bladder, the capsaicin-gated ion channel TRPV1 is expressed both within afferent nerve terminals and within the epithelial cells that line the bladder lumen. | |||||||||||||||
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We summarize disease-related changes in TRPV1 expression and its implications for therapy and potential adverse effects. | |||||||||||||||
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Heterologously expressed VR1 can be activated by vanilloid compounds, protons, or heat (>43 degrees C), but whether this channel contributes to chemical or thermal sensitivity in vivo is not known. | |||||||||||||||
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In patch-clamp experiments, capsiate was found to activate TRPV1 expressed transiently in HEK293 cells with a similar potency as capsaicin. | |||||||||||||||
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The vanilloid receptor-1 (VR1) is a ligand-gated, non-selective cation channel expressed predominantly by sensory neurons. | |||||||||||||||
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The vanilloid receptor-1 (VR1) is a ligand-gated, non-selective cation channel expressed predominantly by sensory neurons. | |||||||||||||||
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In response to I-RTX in vitro, HEK293 cells expressing rat TRPV1 exhibited increases in intracellular Ca(2+) (biphasic, EC(50) = 56.7 nM and 9.9 microM) that depended on Ca(2+) influx and outwardly rectifying, capsazepine-sensitive currents that were smaller than those evoked by 1 microM capsaicin. | |||||||||||||||
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General Comments
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