We asked why liability for epileptogenesis of hippocampus is increasing along its longitudinal axis. Transverse slices of ventral hippocampus (VHS) bathed in normal medium presented a persistent spontaneous synchronous activity depended on several neurotransmitter systems and electric synapses. It consisted of 1–6 Hz recurrence of field waves underlied by GABA-A and Cl-mediated IPSPS of pyramidal neurons (PN). No such activity was observed in slices of dorsal H (DHS). While intrinsic properties of CA1 PN were comparable, in VHS their excitatory synapses from CA3 appeared to possess a higher release probability, the EPSPs decay phase was relatively slower (by 110%) and recurrent inhibition was weaker. Furthermore VHS were more susceptible to the pharmacological induction of epileptiform discharges (ED). Perfused with [Mg++]-free medium VHS displayed ED with greater incidence, duration and frequency. Adding NMDA further enhanced ED and NMDA antagonists shortened ED more in VHS than in DHS. For at least one hour after washout with normal medium 61% of VHS and only 9.5% of DHS displayed persistent spontaneous ED. These data suggest that the relatively greater epileptogenicity of ventral hippocampus depends on factors intrinsic to small hippocampal circuits which can be maintained in vitro, including weaker inhibition, greater propensity for field synchronization and epileptogenesis and greater involvement of NMDA receptors activation.