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为探讨癫痫发病的生物化学机制，用培养的大鼠大脑皮层神经元和大脑皮层匀浆及突触膜为模型，采用酶联免疫法，放射分析法观察马桑内酯（ＣＬ）对大鼠脑内γ－氨基丁酸（ＧＡＢＡ）分泌，谷氨酸脱梭酶（ＧＡＤ）活性和谷氨酸（Ｇｌｕ）受体结合力的影响。结果表明，５０μｍｏｌ／ＬＣＬ可抑制ＧＡＢＡ分泌，１２、２４、４８小时抑制率为８．３％～１４。５％；在０．１５～１５０μｍｏｌ／Ｌ范围，ＣＬ可抑制ＧＡＤ活性，抑制率为１．３２％～１８．７６％；ＣＬ在２．８～３５０μｍｏｌ／Ｌ范围内可降低Ｇｌｕ受体结合力，降低程度为１８．８％～３１．６％，且各剂量组与对照组差异均有极显著意义（Ｐ＜０．０１）。证实ＣＬ可抑制培养神经元ＧＡＢＡ分泌，并呈时间依赖和剂量依赖关系。
To explore the biochemical mechanism of epilepsy, the cultured rat cerebral cortical neurons and cerebral cortex homogenate and synaptic membrane as a model, enzyme-linked immunosorbent assay and radiological analysis were used to observe the effect of CL Brain GABA secretion, GAD activity and glutamate (Glu) receptor binding. The results showed that 50μmol / L LCA could inhibit the secretion of GABA, and the inhibitory rate was 8.3% ~ 14.5% at 12, 24 and 48 hours. In the range of 0.15 ~ 150μmol / L, .32% ~ 18.76%. In the range of 2.8 ~ 350μmol / L, CL decreased the binding capacity of Glu receptor by 18.8% ~ 31.6%, and the difference between each dose group and the control group There was a significant difference (P <0.01). Confirmed that CL can inhibit neuronal GABA secretion in a time-dependent and dose-dependent manner.