Capsaicin Blocks the Hyperpolarization-Activated Inward Currents via TRPV1 in the Rat Dorsal Root Ganglion Neurons

Capsaicin, the pungent ingredient in hot pepper, activates nociceptors to produce pain and inflammation. However, prolonged exposures of capsaicin will cause desensitization to nociceptive stimuli. Hyperpolarization-activated cation currents (Ih) contribute to the maintenance of the resting membrane...

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Main Author:	Kwak, Jiyeon
Format:	Online
Language:	English
Published:	The Korean Society for Brain and Neural Science 2012
Online Access:	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3381215/

id	pubmed-3381215
recordtype	oai_dc
spelling	pubmed-33812152012-07-12 Capsaicin Blocks the Hyperpolarization-Activated Inward Currents via TRPV1 in the Rat Dorsal Root Ganglion Neurons Kwak, Jiyeon Original Article Capsaicin, the pungent ingredient in hot pepper, activates nociceptors to produce pain and inflammation. However, prolonged exposures of capsaicin will cause desensitization to nociceptive stimuli. Hyperpolarization-activated cation currents (Ih) contribute to the maintenance of the resting membrane potential and excitability of neurons. In the cultured dorsal root ganglion (DRG) neurons, we investigated mechanisms underlying capsaicin-mediated modulation of Ih using patch clamp recordings. Capsaicin (1 µM) inhibited Ih only in the capsaicin-sensitive neurons. The capsaicin-induced inhibition of Ih was prevented by preexposing the TRPV1 antagonist, capsazepine (CPZ). Capsaicin-induced inhibition of Ih was dose dependent (IC50= 0.68 µM) and partially abolished by intracellular BAPTA and cyclosporin A, specific calcineurin inhibitor. In summary, the inhibitory effects of capsaicin on Ih are mediated by activation of TRPV1 and Ca2+-triggered cellular responses. Analgesic effects of capsaicin have been thought to be related to desensitization of nociceptive neurons due to depletion of pain-related substances. In addition, capsaicin-induced inhibition of Ih is likely to be important in understanding the analgesic mechanism of capsaicin. The Korean Society for Brain and Neural Science 2012-06 2012-06-12 /pmc/articles/PMC3381215/ /pubmed/22792028 http://dx.doi.org/10.5607/en.2012.21.2.75 Text en Copyright © Experimental Neurobiology 2012. http://creativecommons.org/licenses/by-nc/3.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
repository_type	Open Access Journal
institution_category	Foreign Institution
institution	US National Center for Biotechnology Information
building	NCBI PubMed
collection	Online Access
language	English
format	Online
author	Kwak, Jiyeon
spellingShingle	Kwak, Jiyeon Capsaicin Blocks the Hyperpolarization-Activated Inward Currents via TRPV1 in the Rat Dorsal Root Ganglion Neurons
author_facet	Kwak, Jiyeon
author_sort	Kwak, Jiyeon
title	Capsaicin Blocks the Hyperpolarization-Activated Inward Currents via TRPV1 in the Rat Dorsal Root Ganglion Neurons
title_short	Capsaicin Blocks the Hyperpolarization-Activated Inward Currents via TRPV1 in the Rat Dorsal Root Ganglion Neurons
title_full	Capsaicin Blocks the Hyperpolarization-Activated Inward Currents via TRPV1 in the Rat Dorsal Root Ganglion Neurons
title_fullStr	Capsaicin Blocks the Hyperpolarization-Activated Inward Currents via TRPV1 in the Rat Dorsal Root Ganglion Neurons
title_full_unstemmed	Capsaicin Blocks the Hyperpolarization-Activated Inward Currents via TRPV1 in the Rat Dorsal Root Ganglion Neurons
title_sort	capsaicin blocks the hyperpolarization-activated inward currents via trpv1 in the rat dorsal root ganglion neurons
description	Capsaicin, the pungent ingredient in hot pepper, activates nociceptors to produce pain and inflammation. However, prolonged exposures of capsaicin will cause desensitization to nociceptive stimuli. Hyperpolarization-activated cation currents (Ih) contribute to the maintenance of the resting membrane potential and excitability of neurons. In the cultured dorsal root ganglion (DRG) neurons, we investigated mechanisms underlying capsaicin-mediated modulation of Ih using patch clamp recordings. Capsaicin (1 µM) inhibited Ih only in the capsaicin-sensitive neurons. The capsaicin-induced inhibition of Ih was prevented by preexposing the TRPV1 antagonist, capsazepine (CPZ). Capsaicin-induced inhibition of Ih was dose dependent (IC50= 0.68 µM) and partially abolished by intracellular BAPTA and cyclosporin A, specific calcineurin inhibitor. In summary, the inhibitory effects of capsaicin on Ih are mediated by activation of TRPV1 and Ca2+-triggered cellular responses. Analgesic effects of capsaicin have been thought to be related to desensitization of nociceptive neurons due to depletion of pain-related substances. In addition, capsaicin-induced inhibition of Ih is likely to be important in understanding the analgesic mechanism of capsaicin.
publisher	The Korean Society for Brain and Neural Science
publishDate	2012
url	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3381215/
_version_	1611538571499405312

Capsaicin Blocks the Hyperpolarization-Activated Inward Currents via TRPV1 in the Rat Dorsal Root Ganglion Neurons

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