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实验在70只乌拉坦麻醉的SD大鼠上进行。在海马CA3区记录诱发的群体锋电位（PS）,探讨了左旋精氨酸——氧化氮（L-Arg-NO）途径对铝抑制PS波幅的作用。结果:（1）0.5 mol/L AICI_3注入CA3区后,PS幅度较注药前显著减小（P<0.05）。（2）CA3区内注入0.1和 0.3mol/L硝基左旋精氨酸（ NLA）能分别加强0.25和0.5 mol/L AICl_3 的抑制效应。（3）CA3区注入0.3 mol/L左旋精氨酸（L-Arg）能拮抗0.5 mol/L AICI_3 对PS波幅的抑制作用,此拮抗作用并能为 NLA所翻转。（4）CA3区内注入 0.2mmol/L亚甲蓝（MB）能加强铝对PS的抑制作用。结果提示:AICI_3对CA3区诱发的PS幅度有抑制作用,此作用可能与L-Arg-NO途径受到损害有关。
The experiment was performed on 70 urethane anesthetized SD rats. The induced population spike potential (PS) was recorded in hippocampal CA3 region and the effect of L-arginine-nitric oxide (L-Arg-NO) pathway on aluminum inhibition of PS amplitude was also investigated. Results: (1) After 0.5 mol / L AICI_3 was injected into CA3 region, the amplitude of PS was significantly decreased (P <0.05). (2) Injection of 0.1 and 0.3 mol / L nitro-L-arginine (NLA) into CA3 region could enhance the inhibitory effect of AICl_3 at doses of 0.25 and 0.5 mol / L, respectively. (3) 0.3 mol / L L-arginine (L-Arg) injected into CA3 area could antagonize the inhibitory effect of 0.5 mol / L AICI_3 on PS amplitude, and this antagonism could be reversed by NLA. (4) Injection of 0.2mmol / L methylene blue (MB) into CA3 region can enhance the inhibitory effect of aluminum on PS. The results suggest that: AICI_3 on the CA3-induced PS amplitude inhibition, the role may be related to the L-Arg-NO pathway compromised.