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Ginkgo biloba extracts inhibit post-ischemic LTP through attenuating EPSCs in rat hippocampus
Metabolic Brain Disease ( IF 3.2 ) Pub Date : 2021-08-31 , DOI: 10.1007/s11011-021-00830-4
Yong Liu 1, 2, 3 , Supeng Ding 1 , Yifei Luan 1, 3 , Zhichao Zhu 1 , Yuting Cai 1 , Yingkui Liu 1, 3
Affiliation  

Ginkgo biloba extract 761 (EGb761), a standardized extract from the Ginkgo biloba leaf, is purported to inhibit NMDA receptor-mediated neuronal excitotoxicity and protect neurons form ischemic injury. However, the specific signal pathway involved in the effects of EGb761 on synaptic plasticity is still in dispute. In this article, effects of EGb761 and its monomer component ginkgolide A (GA), ginkgolide B (GB), ginkgolide C (GC) and quercetin on rat hippocampal synaptic plasticity were studied. The evoked Excitatory postsynaptic currents (EPSCs) and miniature EPSCs were recorded on hippocampal slices from SD rats (14–21 days of age) by whole-cell patch-clamp recording and long-term potentiation (LTP) was induced by theta-burst stimulation. Acutely applied EGb761 inhibited the LTP, but bilaterally affect the evoked EPSCs. The evoked EPSCs were increased by incubation of lower concentration of EGb761, then the evoked EPSCs were decreased by incubation of higher concentration of EGb761. EGb761 monomer component GA, GB and GC could also inhibit the TBS-induced LTP and EPSC amplitude but not paired-pulse ratio (PPR). But quercetin, another monomer component of EGb761, led to increase in EPSC amplitude and decrease in PPR. Simultaneously, EGb761 and its monomer component ginkgolides inhibited the post-ischemic LTP (i-LTP) by inhibiting the EPSCs and the AMPA receptor subunit GluA1 expression on postsynaptic membrane. The results indicated that high concentration of EGb761 might inhibit LTP and i-LTP through inhibition effects of GA, GB and GC on AMPA receptors.



中文翻译:

银杏叶提取物通过减弱大鼠海马 EPSCs 抑制缺血后 LTP

银杏叶提取物 761 (EGb761) 是一种来自银杏叶的标准化提取物,据称可抑制 NMDA 受体介导的神经元兴奋性毒性并保护神经元免受缺血性损伤。然而,EGb761对突触可塑性的影响所涉及的特定信号通路仍存在争议。本文研究了EGb761及其单体成分银杏内酯A(GA)、银杏内酯B(GB)、银杏内酯C(GC)和槲皮素对大鼠海马突触可塑性的影响。通过全细胞膜片钳记录在 SD 大鼠(14-21 天龄)的海马切片上记录诱发的兴奋性突触后电流 (EPSCs) 和微型 EPSCs,并通过 theta-burst 刺激诱导长时程增强 (LTP) . 急性应用 EGb761 抑制 LTP,但对诱发的 EPSCs 有双边影响。通过孵育较低浓度的EGb761,诱发的EPSCs增加,然后通过孵育较高浓度的EGb761,诱发的EPSCs减少。EGb761单体成分GA、GB和GC也可以抑制TBS诱导的LTP和EPSC振幅,但不能抑制双脉冲比(PPR)。但是EGb761的另一种单体成分槲皮素导致EPSC振幅增加和PPR降低。同时,EGb761及其单体成分银杏内酯通过抑制EPSCs和AMPA受体亚基GluA1在突触后膜上的表达来抑制缺血后LTP(i-LTP)。结果表明,高浓度EGb761可能通过GA、GB和GC对AMPA受体的抑制作用抑制LTP和i-LTP。然后通过孵育更高浓度的EGb761,诱发的EPSCs减少。EGb761单体成分GA、GB和GC也可以抑制TBS诱导的LTP和EPSC振幅,但不能抑制双脉冲比(PPR)。但是EGb761的另一种单体成分槲皮素导致EPSC振幅增加和PPR降低。同时,EGb761及其单体成分银杏内酯通过抑制EPSCs和AMPA受体亚基GluA1在突触后膜上的表达来抑制缺血后LTP(i-LTP)。结果表明,高浓度EGb761可能通过GA、GB和GC对AMPA受体的抑制作用抑制LTP和i-LTP。然后通过孵育更高浓度的EGb761,诱发的EPSCs减少。EGb761单体成分GA、GB和GC也可以抑制TBS诱导的LTP和EPSC振幅,但不能抑制双脉冲比(PPR)。但是EGb761的另一种单体成分槲皮素导致EPSC振幅增加和PPR降低。同时,EGb761及其单体成分银杏内酯通过抑制EPSCs和AMPA受体亚基GluA1在突触后膜上的表达来抑制缺血后LTP(i-LTP)。结果表明,高浓度EGb761可能通过GA、GB和GC对AMPA受体的抑制作用抑制LTP和i-LTP。EGb761 的另一种单体成分导致 EPSC 振幅增加和 PPR 降低。同时,EGb761及其单体成分银杏内酯通过抑制EPSCs和AMPA受体亚基GluA1在突触后膜上的表达来抑制缺血后LTP(i-LTP)。结果表明,高浓度EGb761可能通过GA、GB和GC对AMPA受体的抑制作用抑制LTP和i-LTP。EGb761 的另一种单体成分导致 EPSC 振幅增加和 PPR 降低。同时,EGb761及其单体成分银杏内酯通过抑制EPSCs和AMPA受体亚基GluA1在突触后膜上的表达来抑制缺血后LTP(i-LTP)。结果表明,高浓度EGb761可能通过GA、GB和GC对AMPA受体的抑制作用抑制LTP和i-LTP。

更新日期:2021-08-31
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