左乙拉西坦对马桑内酯致痫海马神经细胞钠电流的影响

Effect of Levetiracetam on the Sodium Currents of Rat Hippocampal Neurons Exposed to Coriaria Lactone

目的探讨左乙拉西坦(Levetiracetam,LEV)对马桑内酯(coriaria lactone,CL)致痫SD大鼠海马神经元钠电流增加的影响。方法利用膜片钳全细胞模式,记录急性分离后CL致痫的大鼠海马神经元钠电流,并给予LEV进行干预,分为对照组、LEV 150μmol/L组、LEV 300μmol/L组和未处理组。另用LEV 300μmol/L预处理40 min后再给予CL致痫,观察钠电流的变化情况。结果CL致痫后钠电流增加,加入LEV 150μmol/L后最大电流峰值增加了36.92%±2.84%(P<0.05),与未处理组比较差异无统计学意义(P>0.05)。LEV 300μmol/L组钠电流增加了16.58%±1.56%(P>0.05);但与对照组相比,差异无统计学意义(P>0.05)。经LEV预处理后,CL仍使钠电流增加了32.86%±6.73%(P<0.05),与未处理组比较差异无统计学意义(P>0.05)。结论LEV未能抑制CL致痫海马细胞钠电流的增加,其抗癫痫作用可能不是通过抑制钠电流而产生的。

Objective To test the effect of Levetiracetam（LEV） on the sodium currents of rat hippocampal neurons exposed to epileptogenic coriaria lactone（CL）.Methods Acutely isolated Sprague-Dawley Rat hippocampal neurons were subjected to the whole-cell mode of patch clamp under experimental conditions designed to detect voltage-gated sodium currents.The CL（0.2 mg/mL） was used to increase the sodium currents of the neurons.Then the LEV was added（150 or 300 μmol/L） to test the effect of LEV on the peak current amplitudes through a comparison with the control group in which extracellular solution was added instead and the group in which nothing was added.Another group was pretreated with 300 μmol/L of LEV before the neutrons were treated with the CL.Results The maximum peak amplitudes（MPA） of the sodium currents increased 36.92%±2.84% by the 150 μmol/L of LEV（P〈0.05）,similar to those exposed to the CL only（P〉0.05）.The increase of MPA of the sodium currents by the 300 μmol/L of LEV（16.58%±1.56%） was less than those exposed to the CL only（P〈0.05）.However,no significant difference was found between the 300 μmol/L LEV treated group and the control group（P〉0.05）.The MPA of the sodium currents of LEV pretreated neutrons increased 32.86%±6.73% （P〈0.05）,similar to those without pretreatment（P〉0.05）.Conclusion The LEV does not decrease the sodium currents of rat hippocampal neurons induced by the CL.The antiepileptic action of LEV has nothing to do with the neuronal voltage-gated sodium channels.