Xuan Chi X, Xu Z C
Department of Anatomy and Cell Biology, Indiana University School of Medicine, 635 Barnhill Drive, Indianapolis, IN 46202, USA.
Neurosci Lett. 2000 Mar 3;281(1):5-8. doi: 10.1016/s0304-3940(00)00812-0.
Total potassium current in CA1 pyramidal neurons was studied using whole-cell voltage-clamp recording technique in hippocampal slices prepared before and at 6-8 h after transient forebrain ischemia. The total potassium current significantly increased from a control value of 2.17+/-0.17 to 2.96+/-0.31 nA (measured at +70 mV, P<0.05) after ischemia. The slope factor V(c) of activation curve significantly decreased and the half-inactivation voltage V(h) shifted to more depolarized potentials after ischemia. These results indicate that the increase of potassium current might be responsible for the decreased excitability in CA1 neurons after severe ischemia and may be involved in postischemic cell death in hippocampus.
运用全细胞膜片钳记录技术，在短暂性前脑缺血前及缺血后6 - 8小时制备的海马切片中，研究了CA1锥体神经元的总钾电流。缺血后，总钾电流从对照值2.17±0.17显著增加至2.96±0.31 nA（在+70 mV测量，P<0.05）。缺血后，激活曲线的斜率因子V(c)显著降低，半失活电压V(h)向更去极化的电位移动。这些结果表明，钾电流的增加可能是严重缺血后CA1神经元兴奋性降低的原因，并且可能参与海马缺血后细胞死亡。
