论文部分内容阅读
Ca2+-activate chloride current (CACC) plays important physiological roles in different tissues including neuronal system.It is not clear whether there is specificity in CACC activation by Ca2+ from different sources, namely Ca2+ influx through voltage-/ligand-gated Ca2+ channels in the plasma membrane, vs Ca2+ release from intracellular stores.In this study we investigated the activation of CACC by intracellular Ca2+ induced by the membrane depolarization in rat DRG neurons.The whole-cell patch recordings were performed on DRG neurons from 7-day-old SD rat.In the condition of regular external (high [NaCl]) and internal (high [KCl]) solution, brief depolarization evoked a large inward tail current at-80 mV.The depolarization-induced tail current selectively appeared in a subset of medium-diameter DRG neurons and could be partially blocked by chloride current inhibiters DIDS and NFA, indicating a possibly component of CACC.The tail current could also be blocked by Ca2+ free external solution, pretreatment with BAPTA-AM, and NiCl2, indicating Ca2+ influx is essential for the activation of CACC.In fura-2AM-loaded neurons, brief depolarization range from-30 to +90 mV induced a depolarization-dependent increase of intracellular Ca2+.However it seems that the depolarization-induced CACC activation and intracellular Ca2+ increase is not merely a result of opening of voltage-dependent Ca2+ channel.External Na+ and internal K+ also affected the depolarization-induced CACC activation and intracellular Ca2+ increase.Thus the membrane depolarization-induced activation of CACC may use intracellular Ca2+ through Ca2+ channels as well as transporters.