Involvement of Ca_v3.2 T-type Ca²⁺ channels and cystathionine-β-synthase in colitis-related visceral hypersensitivity in mice

We tested the hypothesis that Ca_v3.2 T-type Ca²⁺ channels, which can be rebooted by sulfides from Zn²⁺ inhibition under physiological conditions, and sulfide-generating enzymes including cystathionine-β-synthase (CBS) would participate in the colitis-related visceral pain in mice treated with 2,4,6-trinitrobenzene sulfonic acid (TNBS). The visceral hypersensitivity following TNBS-induced colitis was abolished by an inhibitor or genetic deletion of Ca_v3.2 and by a CBS inhibitor, and accompanied by CBS upregulation in the colon. Our data thus suggest that the enhanced activity of Ca_v3.2 brought about by sulfides generated by upregulated CBS is involved in the colitis-related visceral hypersensitivity.