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目的采用大鼠杏仁核点燃模型研究低频脑深部电刺激的抗癫痫作用及其相关机制。方法首先建立大鼠杏仁核电刺激点燃模型,观察低频脑深部电刺激对其点燃发作的抑制作用,并通过联合应用抗癫痫药物(如丙戊酸钠、尼卡地平等)观察其协同功效。结果低频电刺激(持续刺激15 min,频率为1 Hz,波宽为0.1 ms,强度为100~350μA)能够有效抑制大鼠杏仁核点燃发作(P<0.05);将对杏仁核点燃无明显影响的低能量低频电刺激与低剂量丙戊酸钠或尼卡地平联合应用,发现在抑制杏仁核点燃发作方面具有协同效应,能显著抑制杏仁核点燃发作(P<0.05)。结论低频脑深部电刺激能有效抑制大鼠杏仁核点燃发作,与丙戊酸钠或尼卡地平联用具有协同功效。
Objective To study the antiepileptic effect of low frequency deep brain stimulation in rat amygdaloid nucleus and its related mechanism. Methods The model of electrical stimulation of amygdala was established in rats. The inhibitory effect of low frequency deep brain stimulation on the ignition was observed. The synergistic effect was observed by combination of antiepileptic drugs such as sodium valproate and nicardipine. Results Low-frequency electrical stimulation (continuous stimulation of 15 min, frequency of 1 Hz, wave width of 0.1 ms and intensity of 100-350 μA) could effectively inhibit the onset of amygdala in rats (P <0.05) and had no significant effect on the amygdala Low-power low-frequency electrical stimulation combined with low-dose sodium valproate or nicardipine showed synergistic effect in inhibiting the onset of amygdala, which could significantly inhibit the onset of amygdala (P <0.05). Conclusions Low-frequency deep brain stimulation can effectively inhibit the onset of amygdala in rats and has synergistic effect with sodium valproate or nicardipine.