Capacitance measurements and pH imaging reveal distinct modes of uptake for endocytotic presynaptic membrane and proteins.

Wild-type human recombinant tau protein infused in presynaptic terminals newly assembled microtubules, which sequestered cytosolic dynamins, thereby blocking synaptic vesicle endocytosis and causing activity-dependent rundown of excitatory synaptic transmission in a slice model of mouse brainstem.

The Kv3.3 potassium channel subunit is necessary and sufficient to permit presynaptic location and accelerated repolarisation of the presynaptic action potential, thereby conserving resources and enhancing accuracy of timing information on transmission at the calyx of Held excitatory synapse.

Protein kinase C brings about post-tetanic potentiation - a temporary increase in synaptic strength due to increased transmitter release - via phosphorylation of a target protein, Munc18-1.

Physiologically, vesicle replenishment at the fast calyx synapse requires both fast-endocytosis and scaffold machinery to support rapid neurotransmission, whereas at the slow hippocampal CA1 synapse only endocytosis is necessary.

A novel region in the CaV2.1 α1 subunit regulates coupling of synaptic vesicles to CaV2.1 calcium channels, synaptic vesicle release and docking, and the size of the fast and total releasable pools of synaptic vesicles.

Genetic and electrophysiology experiments provide the first direct evidence that protein kinase C is a calcium-sensing protein in post-tetanic potentiation, a form of synaptic plasticity that supports short-term memory.

The analytic theory establishes the general principles of synaptic transmission, enables extraction of microscopic parameters of synaptic fusion machinery from experiments, and links molecular constituents to synaptic function.

A combination of genetic, electrophysiological, and modeling approaches reveals that presynaptic Rac1 is a key molecule that controls synaptic strength and plasticity by regulating the synaptic vesicle cycle steps controlling the number of fusion competent synaptic vesicles.

Local presynaptic protein synthesis occurring at established nerve terminals in the mammalian brain provides a mechanism for rapidly controlling or restoring presynaptic proteins that affect neurotransmitter release and presynaptic efficiency.