The simultaneous discharge of hippocampal CA3 pyramidal cells is a
widely studied in vitro model of physiological and pathological network
synchronization. This network is rapidly activated because of extensive positive
feedback mediated by recurrent axon collaterals. Here we show that population-burst
duration is limited by depletion of the releasable glutamate pool at these
recurrent synapses. Postsynaptic inhibitory conductances further limit burst
duration but are not necessary for burst termination. The interval between
bursts in vitro depends on the rate of replenishment of releasable
glutamate vesicles and the probability of release of those vesicles at recurrent
synapses. Therefore presynaptic factors controlling glutamate release at recurrent
synapses regulate the probability and duration of synchronous discharges of
the CA3 network.
