Independent osmotic, genetic and biochemical perturbations modulate neurotransmitter release in a multiplicative manner.

A combination of tethered diffusion of release-ready synaptic vesicles and vesicle-vesicle fusion supports neurotransmitter release at the presynaptic active zone of sensory synapses.

Modulation of the energy barrier for membrane fusion is a common mechanism by which sensors in the synapse produce supralinear calcium dependence of vesicle release and short-term synaptic potentiation.

Building on previous work (Diao et al., 2012), we show that the mechanism by which complexin suppresses spontaneous fusion is distinct from the mechanism by which it synchronizes Ca²⁺-triggered fusion.

Munc13 C-terminal domains synergize to coordinate synaptic vesicle docking, priming and fusion.

The mouse rod photoreceptor ribbon creates a large number of releasable vesicles with uniform release kinetics.

Stationary dense-core vesicles depend on the CAPS-1 protein to fuse with the presynaptic membrane.

Single synaptic vesicle imaging shows that kinetically distinct endocytic pathways are differentially regulated by calcium and temperature, and influence the fidelity of synaptic vesicle protein retrieval.

Spontaneous fusion of vesicles at synapses is regulated independently of fusion triggered by action potentials, adding to evidence that the two types of fusion have distinct functions.

A model for synchronous neurotransmitter release suggests that when not in the presence of calcium ions, Synaptotagmin proteins form ring-like structures between the vesicle and plasma membrane that prevent spontaneous fusion.