H2S, a gasotransmitter, enhances Cav3.2 T-type calcium channel activity, and promotes somatic and visceral pain signals. Cav3.2 is considered responsible for the H2S-induced pain signaling, given its inhibition by the pharmacological blockade and genetic knockdown of Cav3.2. Thus, we further examined the role of Cav3.2 in somatic and visceral pain processing, using Cav3.2-KO mice.

CRITICAL ROLE OF CAV3.2 T-TYPE CALCIUM CHANNELS IN H2S-DEPENDENT SOMATIC AND VISCERAL PAIN SIGNALING IN MICE