In mammals, the vesicular glutamate transporter 1 acquired a proline-rich sequence that negatively regulates the spontaneous release of glutamate by reducing the exchange of synaptic vesicles along the axon.
RIM binding UNC-13L C2A domain releases UNC-13L from an autoinhibitory homodimeric complex to become fusion-competent, and regulates probability of synaptic vesicle release in the post-priming process.
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.
In central synapses, the mobility and supply of synaptic vesicles are determined by two independent biological factors: the morphological and structural organization of nerve terminals and the molecular signature of vesicles.
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.