Li Xiaoqing, Hao Xuran, Cheng Bo, Li Xiantao
Ion Channels Lab, Department of Biomedical Engineering, South-Central University for Nationalities, Wuhan, China.
Neuroreport. 2014 May 28;25(8):574-9. doi: 10.1097/WNR.0000000000000137.
In this study, whole-cell recording was carried out to explore the effects of 17β-estradiol on voltage-gated K⁺ (Kv) currents in N2A cells. The acute exposure to 17β-estradiol, in a concentration-dependent manner, significantly inhibited the peak and steady-state currents through Kv channels, showing IC50 values of 3.6 and 3.8 μM, respectively. The reduction in both the amplitude and the decay rate of Kv currents, with an increase in depolarization, suggested that it was a voltage-dependent block. The activation and inactivation experiments were conducted to determine the exact causes of the inhibitory effects. The half-maximum activation potential (V₁/₂) was +8.1 mV in control and remained stable after exposure to 10 μM 17β-estradiol. For steady-state inactivation, the half-maximum inactivation potential (V₁/₂) was -45.0 mV and shifted right to -39.7 mV without a statistical difference, and the time constants of recovery from inactivation were not altered by 17β-estradiol, suggesting that the depression was not correlated with the inactivation gate.
在本研究中，采用全细胞记录法探究17β-雌二醇对N2A细胞中电压门控钾离子（Kv）电流的影响。急性暴露于17β-雌二醇后，其以浓度依赖的方式显著抑制通过Kv通道的峰值电流和稳态电流，IC50值分别为3.6和3.8 μM。随着去极化程度增加，Kv电流的幅度和衰减速率均降低，表明这是一种电压依赖性阻滞。进行激活和失活实验以确定抑制作用的确切原因。对照组的半数最大激活电位（V₁/₂）为+8.1 mV，暴露于10 μM 17β-雌二醇后保持稳定。对于稳态失活，半数最大失活电位（V₁/₂）为-45.0 mV，向右移动至-39.7 mV，但无统计学差异，且从失活状态恢复的时间常数未被17β-雌二醇改变，这表明抑制作用与失活门无关。
