尼卡地平对大鼠杏仁核点燃效应的抑制作用(英文)

目的:探讨钙通道阻滞剂尼卡地平对大鼠杏仁核点燃的作用及机制。方法:恒定电流每日一次刺激大鼠右侧杏仁核,观察尼卡地平对杏仁核点燃发展和发作的影响,测定点燃大鼠脑内各种氨基酸神经递质的含量。结果:腹腔注射尼卡地平2mg·kg~(-1)显著延缓杏仁核点燃发展进程(P<0.01);尼卡地平2-20mg·kg~(-1)剂量依赖性抑制大鼠杏仁核点燃发作,升高发作阈值(ADT),降低Racine分级;20mg·kg~(-1)尼卡地平显著提高杏仁核点燃大鼠脑内抑制性氨基酸神经递质GABA的含量(P<0.05)。结论:尼卡地平对大鼠杏仁核点燃的发展和发作有抑制作用,其机制可能与阻断电压依赖性钙通道及增强GABA系统功能有关。

Inhibition of nicardipine on amygdala kindling in rats

AIM: To investigate the effects and mechanism of nicardipine, a calcium channel blocker, on amygdala kindling in rats. METHODS: Constant current stimulations were delivered to the right amygdala of the rats once a day. The effects of nicardipine on the development and seizure of amygdala kindling were observed and the content of amino acid neurotransmitters in the brain of kindled rats was determined. RESULTS: Nicardipine (2 mg . kg-1, ip) significantly retarded the development of amygdala kindling (P < 0.01); 2 - 20 mg . kg-1 of nicardipine inhibited amygdala kindled seizure dose-dependently, elevated the afterdischarge threshold, and reduced the Racine's stage; 20 mg . kg-1 of nicardipine significantly increased the content of GABA, a kind of inhibitory amino acid neurotransmitter, in the brain of amygdala kindled rats (P < 0.05). CONCLUSION: Nicardipine inhibits amygdala kindling in rats, and the inhibition mechanism may be related to the blockage of the voltage-operated calcium channels and the enhancement of GABAergic system action in the brain.