The different mechanisms of synchronization of epileptic bursts (synaptic) & of the population spikes within them (nonsynaptic) have practical implications for estimating the severity of epileptic responses. Synaptic mechanisms clearly are the key to the functioning of the nervous system. Nevertheless, nonsynaptic interactions between neurons have significant functional & practical consequences that need to be understood. This is particularly important with intense neuronal activity, for instance, during epileptic & other synchronous discharges (Jefferys, 1995). The aim of this work was to evaluate the manifestations & synchronization level of epileptiform events in 3 nonsynaptic epilepsy models.All experiments were performed in accordance with the guidelines set by the National Institutes of Health for the humane treatment of animals and the Animal Care Committee of Bogomoletz Institute of Physiology. The Wistar rats (P12) were deeply anesthetized using sevoflurane & decapitated. Extracellular field potentials were recorded from the CA1 & CA3 pyramidal cell layers of hippocampal slices (500 µm) with glass microelectrodes. Values are means ± SEM, compared by Student’s t-test.For generation of nonsynaptic epileptiform events we perfused slices with ACSF solution contained: a) low Ca2+ or b) Cd2+ (15µM) or c) synaptic transmission blockers (CNQX, 10μM; MK-801, 1µM; bicuculline, 10µM). After application of proepileptic solutions the delay time for epileptiform activity was: a) CA1 – 16±2 min & CA3 – 11±1 min (n=24, p<0.05); b) CA1 – 9±2 min & CA3 – 8±1 min (n=13); c) 9±1 min (n=15) in CA1 & CA3 zones. In response to inhibition of synaptic transmission we observed next manifestations: sigle-, multi-spikes, slow waves with spikes and bursts, burst- and clonic-like activity in CA1 as well as in CA3 area of hippocampus. Worth to note that delay time before epileptic activity is shorter in CA3 area for low Ca2+ & Cd2+ models of epilepsy, while blockade of postsynaptic receptors leads to synchronous start of epileptoform net activity. Reducing the osmolarity of extracellular solution decreases delay time in response to the synaptic blockade.These data suggest that synaptic transmission blockade caused the higher level of epileptiform activity synchronization between CA1 & CA3 comparing with low Ca2+ & Cd2+ models. Thus, other than glutamatergic & gabaergic synaptic transmission systems are involved in epileptiform activity synchronization.