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 Ca_v3.2 T-type Ca²⁺ channels abolishes hydrogen sulfide (H₂S)-mediated pain signals in mice. In Ca_v3.2-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 Ca_v3.2-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 Ca_v3.2 in H₂S-dependent somatic and colonic pain.

Keywords: Ca(v)3.2 T-type calcium channel; Hydrogen sulfide; Pain.