论文部分内容阅读
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。
Objective: To investigate the effect and mechanism of nicardipine, a calcium channel blocker, on the amygdala in rats. Methods: The rat right amygdaloid was stimulated with constant current once a day. The effects of nicardipine on the development of amygdala and the onset of amygdala were observed. The content of various amino acid neurotransmitters in rat brain was measured. Results: Nicardipine 2 mg · kg -1 significantly delayed the development of amygdala (P <0.01). Nicardipine 2 - 20 mg · kg -1 dose-dependently inhibited the amygdala in rats (ADT), and decreased Racine grade. Nicardipine (20 mg · kg -1) significantly increased the content of inhibitory amino acid neurotransmitter GABA (P <0.05) in the brain of amygdala-lighted rats. CONCLUSION: Nicardipine can inhibit the development and onset of amygdala in rats, and its mechanism may be related to blocking voltage-dependent calcium channel and enhancing GABA system function.