Abstract: Objective：To study the molecular basis and the mechanism of volumeactivated chloride currents （VACC） in the satellite glia cells （SGCs） of rat dorsal root ganglion （DRG）. Methods：The VACC was recorded by whole-cell patch clamp technique. Pharmacological tools were used to evaluate the roles of calcium and purinergic receptors in the activation of VACC. siRNA was used to evaluate the role of TMEM16A in the molecular basis of VACC. Results：Hypertonic intracellular solution induced an inward current that was blocked by chloride channel blocker in the SGCs of rat DRG. This current，namely VACC，was reduced significantly when SGCs were transfected with siRNA against TMEM16A. The development of VACC was blocked when the intracellular Ca2+ was chelated with high concentrations of BAPTA or EGTA. VACC was not affected when P2 receptor was blocked. Conclusions：The above results suggest that the SGCs in the rat DRG express VACC. The VACC is activated by the increase of cell volume involving release of intracellular calcium. TMEM16A proteins appear to be a crucial component of the VACC in rat SGCs.

Key words: satellite glia cells, volume-activated chloride channel, Ca2+, trans membrane protein 16A（ TMEM16A）