单剂量和多剂量银杏内酯A的影响,B,C,和白果内酯,银杏叶提取物的活性成分(EGB761),在雄性WAG/Rij大鼠中研究了失神癫痫发作,失神癫痫的遗传动物模型。此外,银杏内酯A与NMDA受体拮抗剂MK-801,AMPA/红藻氨酸受体拮抗剂6-氰基-7-硝基喹喔啉-2,3-二酮(CNQX)的相互作用,或L型钙通道阻滞剂尼卡地平进行了研究,以弄清楚银杏内酯A如何影响大脑中的尖峰波放电(SWDs)。使用6-8个月大的雄性WAG/Rij大鼠进行实验,并植入了输注套管和EEG电极。银杏内酯A,B,C,和白果内酯以6mg/kg的剂量腹膜内给药7天。在互动小组中,6μg银杏内酯A与MK-801(10μg)联合脑室注射,CNQX(1μg),和尼卡地平(50μg)持续7天。在基线时记录动物的脑电图,第一剂,和第七剂量周期为4小时。银杏内酯A(p=.028),C(p=.046),和白果内酯(p=.043)显着增加了WAG/Rij大鼠的SWD频率。用MK-801将银杏内酯A注入侧脑室(p=.046),CNQX(p=.043),和尼卡地平(p=.046)显着增加了第七剂后的SWD数量。最后,EGb761相关的失神癫痫增加被确定为由银杏内酯A引起,C,还有白果内酯.所有三种受体拮抗剂/通道阻断剂均不抑制银杏内酯A的促缺失作用。研究结果表明,银杏内酯A的促缺失作用是由离子型谷氨酸受体或L型钙通道以外的脑回路介导的。
The effects of a single and multiple doses of ginkgolide A, B, C, and bilobalide, active components of Ginkgo biloba extract (EGb 761), on absence seizures were investigated in male WAG/Rij rats, a genetic animal model of absence epilepsy. Furthermore, the interactions of ginkgolide A together with NMDA receptor antagonist MK-801, AMPA/kainate receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), or L-type calcium channel blocker nicardipine were studied to figure out how ginkgolide A affects spike-wave discharges (SWDs) in the brain. The experiments were done using 6-8-month-old male WAG/Rij rats with infusion cannula and EEG electrode implanted. Ginkgolide A, B, C, and bilobalide were administered intraperitoneally for 7 days at a dose of 6 mg/kg. In interaction groups, 6 μg ginkgolide A was injected intracerebroventricularly in combination with MK-801 (10 μg), CNQX (1 μg), and nicardipine (50 μg) for 7 days. EEG was recorded from animals at the baseline, first dose, and seventh dose periods for 4 h. Ginkgolide A (p = .028), C (p = .046), and bilobalide (p = .043) significantly increased the frequency of SWDs in WAG/Rij rats. Ginkgolide A injected into the lateral ventricle with MK-801 (p = .046), CNQX (p = .043), and nicardipine (p = .046) significantly increased the number of SWDs after seventh dose. Finally, the EGb 761-related increase in absence epilepsy was determined to be caused by ginkgolide A, C, and bilobalide. All three receptor antagonists/channel blockers do not inhibit the pro-absence effect of ginkgolide A. The findings revealed that ginkgolide A\'s pro-absence effect is mediated by brain circuits other than ionotropic glutamate receptors or L-type calcium channels.