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Abstract
Excitatory transmission in the vertebrate CNS depends on glutamate release at synapses, activating ionotropic receptors that drive depolarization and calcium influx, triggering intracellular signaling and action potential generation. Presynaptic vesicle release probability (Pr) is influenced by calcium channel properties, vesicle availability, and prior activity. This dissertation focuses on short-term increases in Pr caused by subthreshold somatodendritic depolarizations, which elevate presynaptic calcium and enhance neurotransmitter release.