Genetic deletion of Cav3.2 T-type calcium channels abolishes H2S-dependent somatic and visceral pain signaling in C57BL/6 mice

• Main Authors: Kazuki Matsui (Author), Maho Tsubota (Author), Saaya Fukushi (Author), Nene Koike (Author), Hiroshi Masuda (Author), Yoshihito Kasanami (Author), Takaya Miyazaki (Author), Fumiko Sekiguchi (Author), Tsuyako Ohkubo (Author), Shigeru Yoshida (Author), Yutaro Mukai (Author), Akira Oita (Author), Mitsutaka Takada (Author), Atsufumi Kawabata (Author)
• Format: Book
• Published: Elsevier, 2019-07-01T00:00:00Z.
• Subjects: article
• Online Access: Connect to this object online.

Summary

We tested whether genetic deletion of Cav3.2 T-type Ca2+ channels abolishes hydrogen sulfide (H2S)-mediated pain signals in mice. In Cav3.2-expressing HEK293 cells, Na2S, an H2S donor, at 100 μM clearly increased Ba2+ currents, as assessed by whole-cell patch-clamp recordings. In wild-type C57BL/6 mice, intraplantar and intracolonic administration of Na2S evoked mechanical allodynia and visceral nociceptive behavior, respectively, which were abolished by TTA-A2, a T-type Ca2+ channel blocker. In Cav3.2-knockout mice of a C57BL/6 background, Na2S caused neither somatic allodynia nor colonic nociception. Our study thus provides definitive evidence for an essential role of Cav3.2 in H2S-dependent somatic and colonic pain. Keywords: Hydrogen sulfide, Cav3.2 T-type calcium channel, Pain

Item Description

1347-8613
10.1016/j.jphs.2019.07.010