【摘要】 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更多还原

【Abstract】 In order to investigate the intracellular mechanism of epilepsy induced by L Glutamate(Glu) and antiepilepsy of dexamethasone(Dex), we examined the effect of Dex on [Ca 2+ ] i of the primary cultured hippocampal neurons after reaction of Glu. Loading neurons with Fura 2, [Ca 2+ ] i were measured with EPC 9 light electricity measurement system. The results showed that. (1)[Ca 2+ ] i of neuron was significantly elevated by Glu. The effect was disappeared after loading 5 mmol/L EGTA, which exhauts extracellular Ca 2+ , but it was recovered after administration of CaCl 2 to 1 mmol/L in the medium. The effect was blocked obviously by preloading with 10 μmol/L MK 801(specific and non competitive antagonist of NMDA receptor), but was not blocked in the presence of 10 μmol/L of Verapamil. (2)The effect of Glu was weakened by 100 μmol/L of Dex(2 h). Whereas pretreatment of Dex(100 μmol/L)+Cycloheximide(10 μmol/L, inhibitor of protein synthesis) for 2 h or Dex(100 μmol/L)for 2 min have no effect on [Ca 2+ ] i induced by Glu. These results indicated that Glu could increase [Ca 2+ ] i of hippocampal neuron, depending on extracellular Ca 2+ influx mediated by NMDA receptor. Dex might inhibit the effect of Glu through genomic mechanism.更多还原