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目的研究致癫痫剂马桑内酯对大脑皮质神经元内游离钙（［Ｃａ２＋］ｉ）的作用及其作用途径，以探讨马桑内酯的致癫痫机制。方法利用培养１４天的大鼠大脑皮层神经元和ＡＲ－ＣＭ－ＭＩＣ阳离子检测系统，观察不同浓度的马桑内酯对［Ｃａ２＋］ｉ的作用，并分别用钙通道阻滞剂维拉帕米和２－氨基膦酸基戊酸（ＡＰ５）及钙螯合剂ＥＧＴＡ，观察马桑内酯作用的可能途径。结果马桑内酯使［Ｃａ２＋］ｉ水平升高，在（２５～５００）×１０－６ｍｏｌ／Ｌ范围内，呈明显的剂量效应关系；加入５×１０－３ｍｏｌ／ＬＥＧＴＡ至介质中后，马桑内酯作用消失，补充１０－３ｍｏｌ／Ｌ氯化钙后作用又出现；预先加入５×１０－６ｍｏｌ／Ｌ维拉帕米可明显拮抗其升钙作用，而加入１０－５ｍｏｌ／ＬＡＰ５则阻断作用不明显。结论致癫痫剂马桑内酯可使神经元内［Ｃａ２＋］ｉ升高，其升高［Ｃａ２＋］ｉ的作用依赖于细胞外钙，电压依赖性钙通道可能是其升高［Ｃａ２＋］ｉ的主要途径。
Objective To investigate the effect and mechanism of epileptic agent (docetaxel) on intracellular free calcium ([Ca2 +] i) in cerebral cortex neurons in order to investigate the mechanism of epilepsy caused by epidural. Methods The cultured rat cerebral cortex neurons and AR-CM-MIC cation detection system were used to observe the effects of different concentrations of the prostaglandins on [Ca2 +] i and were treated with verapamil, a calcium channel blocker, And 2-aminophosphonic valeric acid (AP5) and calcium chelator EGTA, the possible ways to observe the effect of coronatone. Results Compared with the control group, there was a dose-response relationship between [Ca2 +] i and (25-500) × 10-6mol / L with the addition of 5 × 10-3mol / L EGTA Sinaldone disappeared, the role of calcium chloride added after 10-3mol / L reappeared; pre-added 5 × 10-6mol / L verapamil significantly antagonized the role of calcium, and added 10-5mol / LAP5 resistance Broken effect is not obvious. CONCLUSIONS: The epileptic agent of docetaxel can increase [Ca2 +] i in neurons, and the effect of [Ca2 +] i on its elevation depends on the extracellular calcium. The voltage-dependent calcium channel may be due to its elevation of [Ca2 +] i main method.