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Ca²⁺-Dependent Mechanisms of Presynaptic Control at Central Synapses

Institute of Neurology, University College London, London, UK

Classically, a high-power association relates the neurotransmitter release probability to the concentration of presynaptic Ca²⁺. Activated by the action potential waveform, voltage-gated Ca²⁺ channels mediate Ca²⁺entry into presynaptic terminals. Inside the terminal, Ca²⁺ ions rapidly bind to endogenous intracellular buffers and could trigger Ca²⁺ release from internal Ca²⁺ stores. The resulting space-time profile of free Ca²⁺ determines the time course and probability of neurotransmitter release through the interaction with molecular release triggers strategically located in the vicinity of release sites. Following a rapid concentration transient, excess Ca²⁺ has to be removed from the cytosol through the process involving Ca²⁺ uptake by the endoplasmatic reticulum stores, sequestration by mitochondria, and/or extrusion into the extracellular medium. The ongoing synaptic activity could affect any of the multiple factors that shape presynaptic Ca²⁺dynamics, thus arbitrating use-dependent modification of the neurotransmitter release probability. Here we present an overview of major players involved in Ca²⁺-dependent presynaptic regulation of neurotransmitter release and discuss the relationships arising between their actions.

Key Words: Synaptic transmission • Presynaptic mechanisms • Plasticity • Calcium signaling

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