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Colonic hydrogen sulfide-induced visceral pain and referred hyperalgesia involve activation of both Ca(v)3.2 and TRPA1 channels in mice.

Abstract：

:Luminal hydrogen sulfide (H(2)S), a gasotransmitter, causes colonic pain / referred hyperalgesia in mice, most probably via activation of T-type Ca(2+) channels. Here we analyzed the mechanisms for H(2)S-induced facilitation of colonic pain signals. Intracolonic administration of NaHS, an H(2)S donor, evoked visceral pain-like nociceptive behavior and referred hyperalgesia in mice, an effect abolished by NNC 55-0396, a selective T-type Ca(2+)-channel blocker, or by knockdown of Ca(v)3.2. AP18, a TRPA1 blocker, also prevented the NaHS-induced colonic pain and referred hyperalgesia. These findings demonstrate that H(2)S-induced colonic pain and referred hyperalgesia require activation of both Ca(v)3.2 and TRPA1 channels in mice.

journal_name

J Pharmacol Sci

journal_title

Journal of pharmacological sciences

authors

Tsubota-Matsunami M,Noguchi Y,Okawa Y,Sekiguchi F,Kawabata A

doi

10.1254/jphs.12086sc

subject

Has Abstract

pub_date

2012-01-01 00:00:00

pages

293-6

issue

3

eissn

1347-8613

issn

1347-8648

pii

DN/JST.JSTAGE/jphs/12086SC

journal_volume

119

pub_type

杂志文章

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