目的：为了在离子通道水平探讨β淀粉样肽（βＡＰ）在Ａｌｚｈｅｉｍｅｒ病中的作用。方法：用７～２１ｄ大鼠，以链霉蛋白酶Ｅ酶解加吸管吹打法制备海马ＣＡ１区神经元；利用全细胞膜片钳技术，观察了βＡＰ２５～３５对急性分离海马ＣＡ１区锥体细胞的短暂性Ｋ＋电流的影响。结果：βＡＰ２５～３５对短暂性Ｋ＋电流有明显抑制作用，且呈明显浓度依赖性、时间依赖性和部分电压依赖性。结论：βＡＰ对Ｋ＋通道的影响在Ａｌｚｈｅｉｍｅｒ病的发生机制中具有重要作用。 Objective: To investigate the role of β-amyloid (βAP) in Alzheimer’s disease at ion channel level. Methods: Neurons in CA1 area of ​​hippocampus were prepared by enzymolysis with Pronase E and pipette in 7-21 days. Whole-cell patch-clamp technique was used to observe the effect of β-AP25-35 on acutely isolated hippocampal CA1 pyramidal neurons Effect of transient K + current on cells. Results: β  AP25 ~ 35 on transient K + current was significantly inhibited, and showed a significant concentration-dependent, time-dependent and partial voltage-dependent. Conclusion: The effect of βAP on K + channels plays an important role in the pathogenesis of Alzheimer’s disease.