Modulation of Presynaptic Store Calcium Induces Release of Glutamate and Postsynaptic Firing

Action potential-independent transmitter release is random and produces small depolarizations in the postsynaptic neuron. This process is, therefore, not thought to play a significant role in impulse propagation across synapses. Here we show that calcium flux through presynaptic neuronal nicotinic receptors leads to mobilization of store calcium by calcium-induced calcium release. Recruitment of store calcium induces vesicular release of glutamate in a manner consistent with synchronization across multiple active zones in the CA3 region of the rat hippocampus. This modulation of action potential-independent release of glutamate is sufficient to drive the postsynaptic pyramidal cell above its firing threshold, thus providing a mechanism for impulse propagation.