Journal
JOURNAL OF PHARMACOLOGICAL SCIENCES
Volume 119, Issue 3, Pages 293-296Publisher
JAPANESE PHARMACOLOGICAL SOC
DOI: 10.1254/jphs.12086SC
Keywords
hydrogen sulfide; T-type calcium channel; TRPA1
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Funding
- Japan Society for the Promotion of Science
- Ministry of Education, Culture, Sports, Science, and Technology
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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 Ca(v)3.2. 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 Ca(v)3.2 and TRPA1 channels in mice.
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