Abstract
The availability of synaptic vesicles (SVs) and their timing for fusion are critical for neurotransmitter release and neural communication. Synapsins (Syn) are abundant phosphoproteins associated reversibly with SVs and cytoskeleton. Syn is highly conserved in animal kingdom and is thought to regulate SVs trafficking and short-term plasticity. Syn function compromises learning and memory, however, its role in synaptic transmission is still under investigation. Here we analyzed Syn null by voltage-clamp recording of synaptic transmission at Drosophila glutamatergic model. We found that Syn null increases the probability of SV fusion by decreasing the sensitivity to calcium. In addition, Syn null increases asynchronous release, alters short-term plasticity and synaptic memory. A use-dependent model for neurotransmission induced by high-frequency nerve activity and a masked plasticity under depression is discussed.
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