低频脑深部电刺激对大鼠杏仁核点燃的抑制作用及其相关机制探讨

The inhibitive effect of low frequency electric brain stimulation on amygdale kindling in rats and its possible mechanisms

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 investigate the effect of low frequency electric deep brain stimulation on amygdale kindling in rats. Methods The amygdale kinkling model of rats was established by operation on the brain, The effects of low frequency deep brain electric stimulation used alone or in combination with anti-epilepsy drugs were observed in terms of severity of seizure attack reflected by Racine＇s scale and afterdischarge duration recorded in electroencephalogram. Results Fifteen minutes of low frequency electric stimulation at 1 Hz and 100 to 350 μA effectively inhibited amygdale kindling as demonstrated by a significant decrease of afterdischarge duration, and decreased the severity of seizure attack （ P 〈 0.05 ）. The combination of low frequency stimulation with valproate sodium or incardipine showed synergic effect. Conclusion Low frequency deep brain stimulation can significantly inhibit amygdala kindling in rats, and has synergic effects with valproate sodium and nicardpine.