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.

In addition, the penultimate sentence in the legend to Fig. 4b was inadvertently omitted. The corrected legend should read: The experiment shown in (a) was repeated in a slice in which CA3 bursting was induced by tetanic stimulation of the CA3 pyramidal cell layer. The average interburst interval in this preparation was 13 seconds, which permitted longer delays between the end of a burst and glutamate application. As in (a), glutamate application at delays closer to the interburst interval triggered a burst more rapidly, but the initial response to glutamate was unchanged (inset). In this cell, bursts triggered calcium escape spikes. Glutamate was applied after every fourth burst in (b) and (c).