Feng Zhouyan, Durand Dominique M
Department of Biomedical Engineering, Zhejiang University, Hangzhou, China.
Epilepsia. 2006 Apr;47(4):727-36. doi: 10.1111/j.1528-1167.2006.00499.x.
It has been shown that a low-calcium high-potassium solution can generate ictal-like epileptiform activity in vitro and in vivo. Moreover, during status epileptiform activity, the concentration of [K+]o increases, and the concentration of [Ca2+]o decreases in brain tissue. Therefore we tested the hypothesis that long-lasting persistent spike activity, similar to one of the patterns of status epilepticus, could be generated by a high-potassium, low-calcium solution in the hippocampus in vivo.
Artificial cerebrospinal fluid was perfused over the surface of the exposed left dorsal hippocampus of anesthetized rats. A stimulating electrode and a recording probe were placed in the CA1 region.
By elevating K+ concentration from 6 to 12 mM in the perfusate solution, the typical firing pattern of low-calcium ictal bursts was transformed into persistent spike activity in the CA1 region with synaptic transmission being suppressed by calcium chelator EGTA. The activity was characterized by double spikes repeated at a frequency approximately 4 Hz that could last for >1 h. The analysis of multiple unit activity showed that both elevating [K+]o and lowering [Ca2+]o decreased the inhibition period after the response of paired-pulse stimulation, indicating a suppression of the after-hyperpolarization (AHP) activity.
These results suggest that persistent status epilepticus-like spike activity can be induced by nonsynaptic mechanisms when synaptic transmission is blocked. The unique double-spike pattern of this activity is presumably caused by higher K+ concentration augmenting the frequency of typical low-calcium nonsynaptic burst activity.
研究表明，低钙高钾溶液在体外和体内均可产生癫痫样痫样活动。此外，在癫痫样状态活动期间，脑组织中细胞外钾离子（[K+]o）浓度升高，细胞外钙离子（[Ca2+]o）浓度降低。因此，我们检验了以下假设：高钾低钙溶液在体内可在海马体中产生类似于癫痫持续状态模式之一的持久持续性棘波活动。
将人工脑脊液灌注到麻醉大鼠暴露的左侧背侧海马体表面。在CA1区放置刺激电极和记录探针。
通过将灌注液中的钾离子浓度从6 mM提高到12 mM，低钙痫样爆发的典型放电模式转变为CA1区的持续性棘波活动，同时钙螯合剂EGTA抑制了突触传递。该活动的特征是双棘波以约4 Hz的频率重复出现，可持续>1小时。多单位活动分析表明，升高[K+]o和降低[Ca2+]o均缩短了配对脉冲刺激反应后的抑制期，表明超极化后（AHP）活动受到抑制。
这些结果表明，当突触传递被阻断时，非突触机制可诱导出类似癫痫持续状态的持续性棘波活动。这种活动独特的双棘波模式可能是由于较高的钾离子浓度增加了典型低钙非突触爆发活动的频率所致。
