Feng Zhouyan, Durand Dominique M
College of Life Science, Zhejiang University, Hangzhou 310027, P.R. China.
Brain Res. 2005 Sep 7;1055(1-2):25-35. doi: 10.1016/j.brainres.2005.06.076.
Recent experiments show that non-synaptic epileptiform activity can be induced by high K+ and low Ca2+ solution in vivo in the hippocampal CA1 region when synaptic transmission is blocked. However, the ability of this type of epileptiform activity to propagate to other brain areas is unknown. Presumably, this epileptiform activity should propagate and project along the axons to remote brain areas. This hypothesis was tested in vivo by inducing non-synaptic seizures in the left hippocampus and by recording spontaneous and evoked field potentials in both left and right hippocampi. The results show that one type of non-synaptic epileptiform activity, late bursts, observed in the left exposed CA1 and CA3 regions could propagate to the contralateral intact CA1 and induce seizures with onsets of high-frequency rhythm. A cut of the commissural fibers near the midline of the brain prevented this propagation. In addition, the measurement of time delays between the exposed left CA3 and contralateral right CA1, as well as between the two recording electrodes in the right CA1, showed that the burst activity propagated through the commissural pathways. Experimental data also showed that these late bursts in the left hippocampus were first generated in the Schaffer collaterals of the CA1 region, traveled to the ipsilateral CA3 region and then propagated through the commissural fibers to the other side. These results suggest that non-synaptic epileptiform activity can propagate along axon projections to intact brain area causing seizure activity. This non-synaptic activity propagating through axonal pathway provides a possible mechanism for the generation of high-frequency low-amplitude onset activity observed commonly in human epileptic EEGs.
最近的实验表明，当突触传递被阻断时，在体内海马CA1区用高钾和低钙溶液可诱导非突触性癫痫样活动。然而，这种类型的癫痫样活动向其他脑区传播的能力尚不清楚。据推测，这种癫痫样活动应该沿着轴突传播并投射到远处的脑区。通过在左侧海马诱导非突触性癫痫发作，并记录左右海马的自发和诱发场电位，在体内对这一假设进行了验证。结果表明，在左侧暴露的CA1和CA3区观察到的一种非突触性癫痫样活动，即晚期爆发，可以传播到对侧完整的CA1区并诱发高频节律发作。在脑中线附近切断连合纤维可阻止这种传播。此外，对暴露的左侧CA3区与对侧右侧CA1区之间以及右侧CA1区两个记录电极之间的时间延迟测量表明，爆发活动通过连合通路传播。实验数据还表明，左侧海马的这些晚期爆发首先在CA1区的Schaffer侧支产生，传播到同侧CA3区，然后通过连合纤维传播到另一侧。这些结果表明，非突触性癫痫样活动可以沿着轴突投射传播到完整的脑区，引起癫痫发作活动。这种通过轴突通路传播的非突触活动为人类癫痫脑电图中常见的高频低幅起始活动的产生提供了一种可能的机制。
