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目的:为了在离子通道水平探讨β淀粉样肽(βAP)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βAP25~35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:βAP25~35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:βAP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 (βAP) 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 βAP on K + channels plays an important role in the pathogenesis of Alzheimer’s disease.