一氧化氮介导麻醉大鼠人参皂苷Rg1诱发长时程增强

目的：研究人参皂苷Rg1对麻醉大鼠突触传递效能的影响及作用机制。方法：应用细胞外微电极录技术，记录麻醉大鼠海马齿状回颗粒细胞群体峰电位（PS）。结果：Rg1(10,100nmol/L)提高麻醉大鼠的基础突触传递，诱导海马齿状回突触传递长时程增强（LTP），并提高高频刺激所诱导的LTP。选择性NOS抑制剂7－硝基吲唑（7－NI，5nmol)侧脑室注射可明显抑制Rg1所诱导的齿状回LTP，对基础突触传递无明显影响。L－Arg(250mg/kg,ip)可拮抗 7－NI对Rg1诱导LTP的抑制作用（P＜0．05）。结论：Rg1显著促进麻醉大鼠的突触传递效能，由神经元型NOS（nNOS）所产生的NO参与了Rg1对齿状回LTP的诱导过程。

NO mediates ginsenoside Rg_1-induced long-term potentiation in anesthetized rats

AIM: To investigate the effect of ginsenoside Rg1 on synaptic transmission in anesthetized rats and the effect of NOS inhibitor, 7-nitroindazole (7-NI), on long-term potentiation (LTP) induced by Rgj. METHODS: Extracellular recording technique was used to record the population spike (PS) in the dentate gyrus (DG) of anesthetized rats. Drug or vehicle injections were delivered via a cannula in the lateral cerebral ventricle. RESULTS: Rg1 (10 and 100 nmol/L) enhanced the basic synaptic transmission and the magnitude of LTP induced by high frequency stimulation (HFS). Selective nNOS inhibitor 7-NI (5 nmol) icv could inhibit the induction of perforant path-dentate gyrus LTP elicited by Rg1( P < 0.05), and L-arginine 250 g/L ip prevented the action of 7-nitroindazole (P < 0.05). CONCLUSION: Rg1-accelerated synaptic transmission and nitric oxide produced by nNOS played a role in the induction of PP-DG LTP in anesthetized rats.