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Synaptic vesicle exocytosis is the biological process by which a synaptic vesicle fuses with the plasma membrane of the pre-synaptic axon terminal and releases its contents into the synaptic cleft. Before exocytosis, neurotransmitter-filled synaptic vesicles are docked at the plasma membrane and primed: exocytosis is triggered by calcium influx.
SNARE-dependent membrane fusion underlies neurotransmission in the nervous system. Here, the authors demonstrate how, in mammalian neurons, the synaptic protein tomosyn controls secretion by increasing the energy barrier for fusion.
How synaptic vesicles (SVs) are clustered at the presynapse is suggestive of anchoring processes counteracting their diffusion. Here, the authors co-track recycling and reserve SVs in live neurons to find that Synapsin 2a tetramerization dynamically immobilizes reserve SVs at the presynapse.
Synaptotagmin (syt) 1 is a calcium sensor for neuronal exocytosis. Here, the authors show that the juxtamembrane linker of this integral membrane protein negatively regulates its calcium sensing activity by mediating self-association via liquid-liquid phase separation.
Life-crucial membrane fusion and budding were traditionally viewed with electron microscopy. With recent breakthroughs that visualize membrane transformation in real time, Wu and Chan synthesize a new model with mechanistic principles and functions.
Synaptotagmin-1 and -7 are calcium sensors that distinctly drive vesicular exocytosis. Here, using wild-type proteins but manipulating the composition of the target membranes, the authors show that synaptotagmin-7 is unusually robust at penetrating membranes.
A computational modelling framework demonstrates how synaptotagmin-1 and −7 can jointly regulate the kinetics and plasticity of neurotransmitter release and provides a powerful tool to test molecular models of calcium-triggered release in silico.
Following synaptic vesicle exocytosis, synaptotagmin 1 recruits a lipid signalling pathway within the presynaptic plasma membrane that drives local dynamin recruitment and membrane retrieval by endocytosis, thus maintaining membrane homeostasis.
In zebrafish, pioneer axons of the dorsal root ganglia require the release of synaptic-like vesicles to enter the spinal cord, suggesting that synaptic vesicles have a role in circuit formation ahead of synaptogenesis.
Super-resolution optical imaging of presynaptic terminals shows that a protein essential to all known forms of neurotransmitter release is clustered in small assemblies that likely correspond to release sites for synaptic vesicle fusion.
Ca2+-independent but voltage-dependent secretion is mediated by the voltage-gated calcium channel subunit CaV2.2, is enabled by SNARE machinery and results in release of ATP or neuropeptide Y.
At hippocampal mossy fibre synapses, depolarization-induced facilitation of vesicle release occurs via a cAMP-dependent increase in coupling between Ca2+ channels and vesicle release machinery.
