PRESYNAPTIC MODULATION OF CA3 NETWORK ACTIVITY

The simultaneous discharge of hippocampal CA3 pyramidal cells is a wid ely studied in vitro model of physiological and pathological network s ynchronization. This network is rapidly activated because of extensive positive feedback mediated by recurrent axon collaterals. Here we sho w that population-burst duration is limited by depletion of the releas able glutamate pool at these recurrent synapses. Postsynaptic inhibito ry conductances further limit burst duration but are not necessary for burst termination. The interval between bursts in vitro depends on th e rate of replenishment of releasable glutamate vesicles and the proba bility of release of those vesicles at recurrent synapses. Therefore p resynaptic factors controlling glutamate release at recurrent synapses regulate the probability and duration of synchronous discharges of th e CA3 network.