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[Activation and regulation of nociceptive transient receptor potential (TRP) channels, TRPV1 and TRPA1].
Yakugaku Zasshi. 2010 Mar; 130(3):289-94.YZ

Abstract

TRP channels are well recognized for their contributions to sensory transduction, responding to a wide variety of stimuli including temperature, nociceptive stimuli, touch, osmolarity and pheromones. In particular, the involvement of TRP channels in nociception has been extensively studied following the cloning of the capsaicin receptor, TRPV1. Painful diabetic peripheral neuropathy is described as a superficial burning pain, and it is one of the most commonly encountered neuropathic pain syndromes in clinical practice. We found that hypoxic and high glucose conditions commonly observed in diabetes potentiate TRPV1 activity without affecting TRPV1 expression both in native rat sensory neurons and HEK293 cells expressing rat TRPV1. The potentiation seems to be caused by phosphorylation of the serine residues of TRPV1 by PKC. These data indicate that PKC-dependent potentiation of TRPV1 activities under hypoxia and hyperglycemia might be involved in early diabetic neuropathy. Mechanisms for the detection of alkaline pH by sensory neurons are not well understood, although it is well accepted that acidic pH monitoring can be attributed to several ion channels, including TRPV1 and ASICs. We found that alkaline pH activates TRPA1 and that the TRPA1 activation is involved in nociception, using Ca(2+)-imaging and patch-clamp methods. In addition, intracellular alkalization activated TRPA1 at the whole-cell level, and single-channel openings were observed in the inside-out configuration. Furthermore, intraplantar injection of ammonium chloride into the mouse hind paw caused pain-related behaviors, which were not observed in TRPA1-deficient mice. These results suggest that alkaline pH causes pain sensation through activation of TRPA1.

Authors+Show Affiliations

Division of Cell Signaling, Okazaki Institute for Integrative Bioscience (National Institute for Physiological Sciences), National Institutes of Natural Sciences, Japan. tominaga@nips.ac.jp

Pub Type(s)

Journal Article
Review

Language

jpn

PubMed ID

20190512

Citation

Tominaga, Makoto. "[Activation and Regulation of Nociceptive Transient Receptor Potential (TRP) Channels, TRPV1 and TRPA1]." Yakugaku Zasshi : Journal of the Pharmaceutical Society of Japan, vol. 130, no. 3, 2010, pp. 289-94.
Tominaga M. [Activation and regulation of nociceptive transient receptor potential (TRP) channels, TRPV1 and TRPA1]. Yakugaku Zasshi. 2010;130(3):289-94.
Tominaga, M. (2010). [Activation and regulation of nociceptive transient receptor potential (TRP) channels, TRPV1 and TRPA1]. Yakugaku Zasshi : Journal of the Pharmaceutical Society of Japan, 130(3), 289-94.
Tominaga M. [Activation and Regulation of Nociceptive Transient Receptor Potential (TRP) Channels, TRPV1 and TRPA1]. Yakugaku Zasshi. 2010;130(3):289-94. PubMed PMID: 20190512.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - [Activation and regulation of nociceptive transient receptor potential (TRP) channels, TRPV1 and TRPA1]. A1 - Tominaga,Makoto, PY - 2010/3/2/entrez PY - 2010/3/2/pubmed PY - 2010/4/30/medline SP - 289 EP - 94 JF - Yakugaku zasshi : Journal of the Pharmaceutical Society of Japan JO - Yakugaku Zasshi VL - 130 IS - 3 N2 - TRP channels are well recognized for their contributions to sensory transduction, responding to a wide variety of stimuli including temperature, nociceptive stimuli, touch, osmolarity and pheromones. In particular, the involvement of TRP channels in nociception has been extensively studied following the cloning of the capsaicin receptor, TRPV1. Painful diabetic peripheral neuropathy is described as a superficial burning pain, and it is one of the most commonly encountered neuropathic pain syndromes in clinical practice. We found that hypoxic and high glucose conditions commonly observed in diabetes potentiate TRPV1 activity without affecting TRPV1 expression both in native rat sensory neurons and HEK293 cells expressing rat TRPV1. The potentiation seems to be caused by phosphorylation of the serine residues of TRPV1 by PKC. These data indicate that PKC-dependent potentiation of TRPV1 activities under hypoxia and hyperglycemia might be involved in early diabetic neuropathy. Mechanisms for the detection of alkaline pH by sensory neurons are not well understood, although it is well accepted that acidic pH monitoring can be attributed to several ion channels, including TRPV1 and ASICs. We found that alkaline pH activates TRPA1 and that the TRPA1 activation is involved in nociception, using Ca(2+)-imaging and patch-clamp methods. In addition, intracellular alkalization activated TRPA1 at the whole-cell level, and single-channel openings were observed in the inside-out configuration. Furthermore, intraplantar injection of ammonium chloride into the mouse hind paw caused pain-related behaviors, which were not observed in TRPA1-deficient mice. These results suggest that alkaline pH causes pain sensation through activation of TRPA1. SN - 0031-6903 UR - https://www.unboundmedicine.com/medline/citation/20190512/[Activation_and_regulation_of_nociceptive_transient_receptor_potential__TRP__channels_TRPV1_and_TRPA1]_ L2 - http://joi.jlc.jst.go.jp/JST.JSTAGE/yakushi/130.289?from=PubMed&lang=en DB - PRIME DP - Unbound Medicine ER -