Li Lin, Liu Zhen-Zhai, He Bing-Jun, Qi Yu
Central Laboratory, the First Hospital, Peking University, Beijing 100034, China.
Zhongguo Yi Xue Ke Xue Yuan Xue Bao. 2008 Jun;30(3):301-4.
To investigate the effect of unaggregated Abeta(25.35) on delayed rectifier potassium current (I(K)) in neonatal rat hippocampal CA3 pyramidal neurons.
The rat hippocampal neurons were enzymatically isolated from 10-11-day-old Wistar rat. The I(K) was recorded using whole-cell patch clamp technique.
The inhibitory effect of unaggregated Abeta(25-35) on I(K) was time-dependent, because I(K) significantly decreased from (6.987 +/- 1.152) nA to (2.540 +/- 0.349) nA after adding unaggregated Abeta(25-35) and reached a stabilized level after 5-7 min (n = 8, P <0.01). However, the inhibitory effect was not concentration-dependent, because the decrease of the I(K) amplitude in different concentration groups were all around 60%. Unaggregated Abeta(25-35) also remarkably affected the half-activation potential, which was (4.114 +/- 0.730) mV and (-5.463 +/- 0.950) mV before and after its application (n = 15, P <0.05); however, the slope factor of activation curve was not significantly changed.
The inhibitory effect of unaggregated Abeta(25-35) on I(K) may be a possible mechanism involved in the pathogenesis of Alzheimer's disease.
研究未聚集的β淀粉样蛋白（25-35）对新生大鼠海马CA3锥体神经元延迟整流钾电流（I(K)）的影响。
从10-11日龄的Wistar大鼠中酶解分离海马神经元。采用全细胞膜片钳技术记录I(K)。
未聚集的β淀粉样蛋白（25-35）对I(K)的抑制作用具有时间依赖性，因为加入未聚集的β淀粉样蛋白（25-35）后，I(K)从（6.987±1.152）nA显著降低至（2.540±0.349）nA，并在5-7分钟后达到稳定水平（n = 8，P <0.01）。然而，抑制作用不具有浓度依赖性，因为不同浓度组的I(K)幅度下降均在60%左右。未聚集的β淀粉样蛋白（25-35）也显著影响半激活电位，应用前为（4.114±0.730）mV，应用后为（-5.463±0.950）mV（n = 15，P <0.05）；然而，激活曲线的斜率因子没有显著变化。
未聚集的β淀粉样蛋白（25-35）对I(K)的抑制作用可能是阿尔茨海默病发病机制中的一个潜在机制。
