Modulation of the hippocampal propensity to non- synaptic epileptiform synchronization in low-calcium model of epilepsy.

The CA3 and CAI regions are the main stages of the "three-synaptic pathway", which plays a role in the generation of hyper-synchronous events in the hippocampus. Under certain experimental conditions, this brain structure might support pathological epileptiform synchronization that is independent of active chemical synaptic transmission. In present work, we estimated the conditions that would facilitate non- synaptic synchronization of the hippocampus. Non-synaptic epileptiform activity was induced in hippocampal slices by the omission calcium ions from the extracellular milieu. The propensity of hippocampal regions to nonsynaptic interactions was estimated by measuring the delay time neededfor the development of low-Ca²⁺ discharges in the CA3 and CAI. Next, an increase of neuronal excitability was induced by the pre- incubation ofhippocampal slices in 4-aminopyridine (4-AP) and by the reduction ofextracellular osmolarity. Pre-incubation of hippbcampal slices with 4-AP under normal osmotic conditions resulted in decreased latency for non-synaptic discharges in the CA3, but not in the CAl. However hypo-osmotic conditions caused increased excitability of the CA3 region, which resulted in decreased delay time for nonsynaptic discharges and this level of cellular excitability was not further enhanced by the pre-incubation with 4-AR.