Synaptophysins and gyrins dampen synaptic strength selectively at low frequencies, hinting that synaptic transmission may play a frequency filtering role in biological computation that is more general than currently envisioned.

The number of neurotransmitter vesicles released into the synaptic cleft is regulated by the size of the readily-releasable pool upstream of release probability.

Synaptic vesicles undergo reversible tethering at the plasma membrane which is activity- and myosin V- dependent.

Clarinet, a novel C. elegans active zone protein with homology to vertebrate Piccolo and Rim, uses its different isoforms for diverse functions, including synaptic vesicle clustering, vesicle release and synaptogenesis.

The precise position of UNC-13 at the active zone near a synapse depends on the N-terminus of the protein, and the C₂A domain in particular, and is essential for accelerating neurotransmitter release.

Drosophila synaptotagmin 7 functions to restrict SV availability and release, but does not act as the Ca²⁺ sensor mediating the asynchronous release and facilitation remaining in synaptotagmin 1 mutants.

Experiments in C. elegans reveal how synaptotagmin and Rab3, the 'yin and yang' of synapses, control whether transmitter vesicles remain docked at the presynaptic membrane or release their contents into the synapse.

The Ca²⁺-dependence of vesicle priming, fusion, and replenishment at cerebellar mossy fiber boutons show a prominent Ca²⁺-dependent priming step, a shallow non-saturating dose-response curve up to 50 µM, and little Ca²⁺-dependence of sustained vesicle replenishment.

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.

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.