Yechikhov Sergey, Shchipakina Tatyana, Savina Tatyana, Kalemenev Sergey, Levin Sergey, Godukhin Oleg
Institute of Theoretical and Experimental Biophysics of Russian Academy of Sciences, Pushchino, Moscow Region, 142290, Russia.
Neurosci Lett. 2002 Dec 19;335(1):21-4. doi: 10.1016/s0304-3940(02)01154-0.
Analysis of extracellular recordings of evoked excitatory postsynaptic potentials and population spikes from rat hippocampal slices has previously revealed that repeated, brief exposures to high extracellular K(+) or to episodes of hypoxia induce a sustained (more than 3 h) hyperexcitability of CA1 pyramidal neurons accompanied with epileptiform activity which was dependent on activation of L-type Ca(2+) channels and N-methyl-D-aspartate receptors. Using in vitro phosphorylation assay we have found the significant increase of Ca(2+)-independent activity of Ca(2+)/calmodulin-dependent protein kinase II in CA1 region of hippocampal slices 60 min after the high extracellular K(+) and 60-80 min after the hypoxic episodes. These data suggest possible involvement of Ca(2+)/calmodulin-dependent protein kinase II in Ca(2+)-dependent mechanisms of the maintenance phase of the observed epileptiform activity.
先前对大鼠海马切片诱发的兴奋性突触后电位和群体锋电位的细胞外记录分析表明，反复、短暂暴露于高细胞外钾离子或缺氧发作会诱导CA1锥体神经元持续（超过3小时）的过度兴奋，并伴有癫痫样活动，这依赖于L型钙通道和N-甲基-D-天冬氨酸受体的激活。使用体外磷酸化测定法，我们发现在高细胞外钾离子处理后60分钟以及缺氧发作后60 - 80分钟，海马切片CA1区钙/钙调蛋白依赖性蛋白激酶II的钙非依赖性活性显著增加。这些数据表明钙/钙调蛋白依赖性蛋白激酶II可能参与了所观察到的癫痫样活动维持阶段的钙依赖性机制。
