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

Abstract

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.

• Authors: Kazuki Matsui, Maho Tsubota, Saaya Fukushi, Nene Koike, Hiroshi Masuda, Yoshihito Kasanami, Takaya Miyazaki, Fumiko Sekiguchi, Tsuyako Ohkubo, Shigeru Yoshida, Yutaro Mukai, Akira Oita, Mitsutaka Takada, Atsufumi Kawabata
• Journal: Journal of pharmacological sciences (J Pharmacol Sci) Vol. 140 Issue 3 Pg. 310-312 (Jul 2019) ISSN: 1347-8648 [Electronic] Japan
• PMID: 31492577 (Publication Type: Journal Article)
• Copyright: Copyright © 2019 The Authors. Production and hosting by Elsevier B.V. All rights reserved.

Chemical References

• Calcium Channel Blockers
• Calcium Channels, T-Type
• TRPA1 Cation Channel
• Calcium
• Hydrogen Sulfide

Topics

• Animals
• Calcium (metabolism)
• Calcium Channel Blockers (pharmacology)
• Calcium Channels, T-Type (genetics, metabolism)
• Cell Line
• HEK293 Cells
• Humans
• Hydrogen Sulfide (pharmacology)
• Mice
• Mice, Inbred C57BL
• Nociceptive Pain (metabolism)
• Rats
• Rats, Wistar
• Signal Transduction (drug effects)
• TRPA1 Cation Channel (metabolism)
• Visceral Pain (metabolism)