为了研究谷氨酸致痫和人工合成的糖皮质激素地塞米松抑痫作用的细胞内机制，本文在ＥＰＣ９ 光电联合检测系统上用Ｆｕｒａ２ 阳离子检测法观察了地塞米松对谷氨酸引起的培养乳鼠海马神经细胞内［Ｃａ２＋ ］ｉ 的影响。结果：（１）谷氨酸引起海马神经元内［Ｃａ２＋ ］ｉ 显著升高，ＥＧＴＡ（５ ｍ ｍ ｏｌ／Ｌ）耗竭细胞外钙后，谷氨酸升钙作用消失，给予氯化钙（１ ｍ ｍ ｏｌ／Ｌ）后其升钙作用恢复：Ｖｅｒａｐａｍ ｉｌ（１０ μｍ ｏｌ／Ｌ）对谷氨酸升钙作用无明显的影响，ＭＫ８０１（１０ μｍ ｏｌ／Ｌ，ＮＭ ＤＡ 受体特异性非竞争性阻断剂）可明显阻断谷氨酸的升钙作用。（２）地塞米松（１００ μｍ ｏｌ／Ｌ）作用２ ｈ 明显抑制了谷氨酸（２００ μｍ ｏｌ／Ｌ）的升钙作用，地塞米松（１００ μｍ ｏｌ／Ｌ）＋ 放线菌酮（１０ μｍ ｏｌ／Ｌ，蛋白合成抑制剂）共同作用２ ｈ，再加入谷氨酸，则地塞米松的抑制作用消失，地塞米松（１００ μｍ ｏｌ／Ｌ）作用２ ｍ ｉｎ 对谷氨酸（２００ μｍ ｏｌ／Ｌ）的升钙作用无明显影响。本实验结果提示，谷氨酸通过ＮＭ ＤＡ 受体介导的外钙内流升高了海马神经元胞内［Ｃａ２＋ ］ｉ，地塞米松可能通过基因组机制抑制了谷氨酸的这种升 In order to study the intracellular mechanism of dexamethasone induced by epilepsy and dexamethasone induced by epilepsy and synthetic glucocorticoid, this paper in the EPC 9 photoelectric detection system with Fura 2 cation detection was observed dexamethasone against glutamic acid Effect of Acid on [Ca2 +] i in Cultured Neonatal Rat Hippocampal Neurons. Results: (1) Glutamate induced a significant increase of [Ca2 +] i in hippocampal neurons and disappeared after EGTA (5 m mol / L) depleted extracellular calcium. Calcium chloride (1 (10 μmol / L) had no obvious effect on the effect of L-glutamate up-regulation. MK801 (10 μmol / L, NMDA receptor specificity Non-competitive blocker) can significantly block the role of glutamic acid calcium. (2) Dexamethasone (100 μmol / L) for 2 h significantly inhibited the uptake of glutamate (200 μmol / L), dexamethasone (100 μmol / L) 10 μmol / L, inhibitor of protein synthesis) for 2 h, then the inhibition of dexamethasone disappeared with the addition of glutamic acid, and the effect of dexamethasone (100 μmol / L) for 2 μm on glutamate 200 μm ol / L) had no significant effect on the uptake of calcium. Our results suggest that glutamate upregulates [Ca2 +] i in hippocampal neurons via NMDA receptor-mediated calcium influx and that dexamethasone may suppress this uptake of glutamate by genomic mechanisms