Suppression of fast GABAergic signalling induces periodic population bursts initiated in the hippocampal CA3 region. We examined the emergence of this activity, the existence of a threshold firing frequency for initiation of bursts and factors underlying initiation at specific sites in the CA3 region. Multi-unit records show that synchronisation of CA3 population discharges induced by bicuculline (10mM) or picrotoxin (50mM) does not emerge suddenly but evolves through partially synchronous activities. They consist of recurring bursts of firing associated with a field potential which increases in amplitude until fully synchronous firing is established. Partially synchronous bursts are terminated by a silent period corresponding to an intracellular hyperpolarisation mediated by GABA_B receptors. During full synchrony, all pyramidal cells discharge during synchronous bursts of duration 50-100 ms. Each burst is preceded by an acceleration of multi-unit firing to a frequency higher than at any other time between bursts. Threshold is modulated by changing cellular excitability or altering excitatory synaptic efficacy and exceeded by induced firing in single pyramidal cells. Extracellular records show that population bursts are always initiated in the CA3a region. Our data suggests that the pacemaker region is defined by both an enhanced recurrent synaptic connectivity and a higher cellular excitability. CA3a cells are more likely to fire discharge in bursts than CA3b cells. Estimates from axonal and dendritic distributions suggest that they receive ~20% more recurrent synapses. CA3a pyramidal cells tend to discharge before population bursts and trigger firing in multi-unit records with a higher probability than CA3b cells so fulfilling two requirements for a pacemaker role.