Colonic Hydrogen Sulfide–Induced Visceral Pain and Referred Hyperalgesia Involve Activation of Both Cav3.2 and TRPA1 Channels in Mice

Luminal hydrogen sulfide (H2S), a gasotransmitter, causes colonic pain / referred hyperalgesia in mice, most probably via activation of T-type Ca2+ channels. Here we analyzed the mechanisms for H2S-induced facilitation of colonic pain signals. Intracolonic administration of NaHS, an H2S donor, evoke...

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Main Authors:	Maho Tsubota-Matsunami, Yumi Noguchi, Yasumasa Okawa, Fumiko Sekiguchi, Atsufumi Kawabata
Format:	Article
Language:	English
Published:	Elsevier 2012-01-01
Series:	Journal of Pharmacological Sciences
Online Access:	http://www.sciencedirect.com/science/article/pii/S1347861319305006

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spelling	doaj-47dd72366e96408cb9afc697eea2702c2020-11-25T02:32:28ZengElsevierJournal of Pharmacological Sciences1347-86132012-01-011193293296Colonic Hydrogen Sulfide–Induced Visceral Pain and Referred Hyperalgesia Involve Activation of Both Cav3.2 and TRPA1 Channels in MiceMaho Tsubota-Matsunami0Yumi Noguchi1Yasumasa Okawa2Fumiko Sekiguchi3Atsufumi Kawabata4Division of Pharmacology and Pathophysiology, Kinki University School of Pharmacy, 3-4-1 Kowakae, Higashi-Osaka, Osaka 577-8502, JapanDivision of Pharmacology and Pathophysiology, Kinki University School of Pharmacy, 3-4-1 Kowakae, Higashi-Osaka, Osaka 577-8502, JapanDivision of Pharmacology and Pathophysiology, Kinki University School of Pharmacy, 3-4-1 Kowakae, Higashi-Osaka, Osaka 577-8502, JapanDivision of Pharmacology and Pathophysiology, Kinki University School of Pharmacy, 3-4-1 Kowakae, Higashi-Osaka, Osaka 577-8502, JapanDivision of Pharmacology and Pathophysiology, Kinki University School of Pharmacy, 3-4-1 Kowakae, Higashi-Osaka, Osaka 577-8502, Japan; Corresponding author. kawabata@phar.kindai.ac.jp on June 28, 2012 (in advance)Luminal hydrogen sulfide (H2S), a gasotransmitter, causes colonic pain / referred hyperalgesia in mice, most probably via activation of T-type Ca2+ channels. Here we analyzed the mechanisms for H2S-induced facilitation of colonic pain signals. Intracolonic administration of NaHS, an H2S donor, evoked visceral pain−like nociceptive behavior and referred hyperalgesia in mice, an effect abolished by NNC 55-0396, a selective T-type Ca2+-channel blocker, or by knockdown of Cav3.2. AP18, a TRPA1 blocker, also prevented the NaHS-induced colonic pain and referred hyperalgesia. These findings demonstrate that H2S-induced colonic pain and referred hyperalgesia require activation of both Cav3.2 and TRPA1 channels in mice. Keywords:: hydrogen sulfide, T-type calcium channel, TRPA1http://www.sciencedirect.com/science/article/pii/S1347861319305006
collection	DOAJ
language	English
format	Article
sources	DOAJ
author	Maho Tsubota-Matsunami Yumi Noguchi Yasumasa Okawa Fumiko Sekiguchi Atsufumi Kawabata
spellingShingle	Maho Tsubota-Matsunami Yumi Noguchi Yasumasa Okawa Fumiko Sekiguchi Atsufumi Kawabata Colonic Hydrogen Sulfide–Induced Visceral Pain and Referred Hyperalgesia Involve Activation of Both Cav3.2 and TRPA1 Channels in Mice Journal of Pharmacological Sciences
author_facet	Maho Tsubota-Matsunami Yumi Noguchi Yasumasa Okawa Fumiko Sekiguchi Atsufumi Kawabata
author_sort	Maho Tsubota-Matsunami
title	Colonic Hydrogen Sulfide–Induced Visceral Pain and Referred Hyperalgesia Involve Activation of Both Cav3.2 and TRPA1 Channels in Mice
title_short	Colonic Hydrogen Sulfide–Induced Visceral Pain and Referred Hyperalgesia Involve Activation of Both Cav3.2 and TRPA1 Channels in Mice
title_full	Colonic Hydrogen Sulfide–Induced Visceral Pain and Referred Hyperalgesia Involve Activation of Both Cav3.2 and TRPA1 Channels in Mice
title_fullStr	Colonic Hydrogen Sulfide–Induced Visceral Pain and Referred Hyperalgesia Involve Activation of Both Cav3.2 and TRPA1 Channels in Mice
title_full_unstemmed	Colonic Hydrogen Sulfide–Induced Visceral Pain and Referred Hyperalgesia Involve Activation of Both Cav3.2 and TRPA1 Channels in Mice
title_sort	colonic hydrogen sulfide–induced visceral pain and referred hyperalgesia involve activation of both cav3.2 and trpa1 channels in mice
publisher	Elsevier
series	Journal of Pharmacological Sciences
issn	1347-8613
publishDate	2012-01-01
description	Luminal hydrogen sulfide (H2S), a gasotransmitter, causes colonic pain / referred hyperalgesia in mice, most probably via activation of T-type Ca2+ channels. Here we analyzed the mechanisms for H2S-induced facilitation of colonic pain signals. Intracolonic administration of NaHS, an H2S donor, evoked visceral pain−like nociceptive behavior and referred hyperalgesia in mice, an effect abolished by NNC 55-0396, a selective T-type Ca2+-channel blocker, or by knockdown of Cav3.2. AP18, a TRPA1 blocker, also prevented the NaHS-induced colonic pain and referred hyperalgesia. These findings demonstrate that H2S-induced colonic pain and referred hyperalgesia require activation of both Cav3.2 and TRPA1 channels in mice. Keywords:: hydrogen sulfide, T-type calcium channel, TRPA1
url	http://www.sciencedirect.com/science/article/pii/S1347861319305006
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Colonic Hydrogen Sulfide–Induced Visceral Pain and Referred Hyperalgesia Involve Activation of Both Cav3.2 and TRPA1 Channels in Mice

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