We tested the hypothesis that Ca3.2 T-type Ca channels, which can be rebooted by sulfides from Zn 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 Ca3.2 and by a CBS inhibitor, and accompanied by CBS upregulation in the colon. Our data thus suggest that the enhanced activity of Ca3.2 brought about by sulfides generated by upregulated CBS is involved in the colitis-related visceral hypersensitivity.
