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目的：研究地塞米松（Ｄｅｘ）对神经元和胶质细胞内钙浓度（［Ｃａ２＋］ｉ）的影响．方法：Ｆｕｒａ２ＡＭ负载小鼠海马细胞（ＮＭＨＣ）和培养的胶质细胞（ＣＣＮ）．单细胞内［Ｃａ２＋］ｉ由ＡＲＣＭＭＩＣ检测系统测定．结果：Ｄｅｘ使多数ＮＭＨＣ［Ｃａ２＋］ｉ浓度依赖地迅速升高，９６个ＮＭＨＣ中仅１０％出现［Ｃａ２＋］ｉ降低．［Ｃａ２＋］ｉ升高被无镁细胞外液阻滞、被氯化镧逆转，但不受氯化锂影响．无钙Ｈａｎｋｓ液悬浮、米非司酮（Ｍｉｆ）或河毒素均可阻断Ｄｅｘ４０－９０μｍｏｌ·Ｌ－１的升［Ｃａ２＋］ｉ效应，而Ｄｅｘ２００μｍｏｌ·Ｌ－１的效应仍被保持．４０个ＣＣＮ中５０％对Ｄｅｘ产生浓度依赖的［Ｃａ２＋］ｉ升高，并被无钙或无镁的细胞外液和Ｍｉｆ预处理抑制．结论：Ｄｅｘ快速改变海马神经元和胶质细胞内［Ｃａ２＋］ｉ．［Ｃａ２＋］ｉ的这种改变是由Ｍｇ２＋和受体相关的外钙内流及高浓度Ｄｅｘ诱发的内钙释放介导的．
AIM: To investigate the effect of dexamethasone (Dex) on the intracellular calcium concentration ([Ca2 +] i) in neurons and glial cells. Methods: Fura2 AM loaded mouse hippocampal cells (NMHC) and cultured glial cells (CCN). Single intracellular [Ca2 +] i by the ARCMIC detection system. RESULTS: Dex caused a sharp increase in concentration of most of the NMHC [Ca2 +] i, with a decrease of [Ca2 +] i in only 10% of the 96 NMHs. The increase of [Ca2 +] i was blocked by magnesium-free extracellular fluid and reversed by lanthanum chloride but not affected by lithium chloride. Calcium-free Hanks’ suspension, Mif or tetrodotoxin blocked the effect of Dex40-90μmol·L-1 [Ca2 +] i, while the effect of Dex200μmol·L-1 was still maintained. 50% of 40 CCNs had a concentration-dependent [Ca2 +] i increase in Dex, and were inhibited by pretreatment with either calcium-free or magnesium-free extracellular fluid and Mif. Conclusion: Dex rapidly changes [Ca2 +] i in hippocampal neurons and glial cells. This change in [Ca2 +] i is mediated by Ca2 + release mediated by Mg2 + and receptor-related calcium influx and high concentration of Dex.