Abstract
An action potential triggers neurotransmitter release from synaptic vesicles docking to a specialized release site of the presynaptic plasma membrane, the active zone. The active zone is a highly organized structure with proteins that serves as a platform for synaptic vesicle exocytosis, mediated by SNAREs complex and Ca2+ sensor proteins, within a sub-millisecond opening of nearby Ca2+ channels with the membrane depolarization. In response to incoming neuronal signals, each active zone protein plays a role in the release-ready site replenishment with synaptic vesicles for sustainable synaptic transmission. The active zone release apparatus provides a possible link between neuronal activity and plasticity. This review summarizes the mostly physiological role of active zone protein interactions that control synaptic strength, presynaptic short-term plasticity, and homeostatic synaptic plasticity.
Highlights
Synaptic transmission is initiated by the fusion of neurotransmitter-containing synaptic vesicles (SVs) with the presynaptic plasma membrane
ELKS has differential, synapse-specific effects on the readily releasable pool (RRP) (SV docking) and the release probability (SV priming), it is proposed that ELKS N-terminal domains have important roles in SV priming [70]
At the hippocampal CA3-to-CA1 synapse and the granule cell parallel fiber (PF)-to-Purkinje cell (PC) synapse of a knock-in mouse, in which all Munc18-1 Protein kinase C (PKC) phosphorylation sites were eliminated, 70% of post-tetanic potentiation (PTP) remained at CA3-toCA1 synapses, and the amplitude of PTP was not reduced at PF-to-PC synapses [84]
Summary
Synaptic transmission is initiated by the fusion of neurotransmitter-containing synaptic vesicles (SVs) with the presynaptic plasma membrane. I further discuss Ca2+ dynamics-dependent replenishment of the neurotransmitter release site with release-ready SVs that involves multiple protein cascades, such as calmodulin-binding [9] and phosphorylation and dephosphorylation of AZ proteins [10,11]. These protein reactions underlie the presynaptic short-term plasticity [9,12,13] and homeostatic synaptic plasticity [14,15,16]. The AZ release apparatus provides a possible link between neuronal activity and sustainable synaptic transmission
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