Propagation of low calcium non-synaptic induced epileptiform activity to the contralateral hippocampus in vivo.

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.