MrgD is expressed almost exclusively in dorsal root ganglion(DRG) neurons.And its activation inhibited KCNQ/M-currents that contributes to an increase in excitability of DRG neurons and thus may enhance the signaling of primary afferent nociceptive neurons.Ca2+-activated chloride channels(CaCCs) are found in DRG neurons and regulate neuronal cell excitability as well.But the interaction between CaCCS and MrgD is still unknown.We here found that β-alanine-induced activation of MrgD resulted in eliciting Ca2+-activated chloride currents.The currents were inhibited by flufenamic acid(FFA) and by inhibition of phospholipase C and Ca2+ chelating agent EGTA.However,calphostin C,a PKC inhibitor,had no effect on the currents.These present data show that the inward currents induced by activation of MrgD were mediated through Gq-phospholipase C-IP3-Ca2+ release pathway,but not via Gi pathway. It is almost exclusively in dorsal root ganglion (DRG) neurons. And its activation inhibited KCNQ / M-currents that contributes to an increase in excitability of DRG neurons and thus may enhance the signaling of primary afferent nociceptive neurons. Ca2 + -activated chloride channels (CaCCs) are found in DRG neurons and regulate neuronal cell excitability as well. But the interaction between CaCCS and MrgD is still unknown. We found found that β-alanine-induced activation of MrgD resulted in eliciting Ca2 + -activated chloride currents. were inhibited by flufenamic acid (FFA) and by inhibition of phospholipase C and Ca2 + chelating agent EGTA.However, calphostin C, a PKC inhibitor, had no effect on the currents. se present data show that the inward currents induced by activation of MrgD were mediated through Gq-phospholipase C-IP3-Ca2 + release pathway, but not via Gi pathway.