An implantable device based on organic electrochemical transistors is developed for quantitative mapping of neurotransmitter release across multiple brain regions, revealing a cross-talk between the mesolimbic and nigrostriatal dopaminergic pathways.

The crystal structure of a large C-terminal fragment of Munc13-1 provides a key framework to understand how Munc13-1 mediates neurotransmitter release and presynaptic plasticity.

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

Cryo-electron tomography, reconstitution, and electrophysiological data show that a fundamental function of Munc13-1 is to bridge synaptic vesicles to the presynaptic plasma membrane.

Naturally-occurring v-SNARE TMD variants differentially regulate fusion pore dynamics and cooperate with phospholipids in supporting membrane curvature at the fusion pore neck.

Challenging a widespread model, biophysical and electrophysiological experiments suggest a new mechanism whereby complexins inhibit neurotransmitter release through electrostatic repulsion between their accessory helix and the membranes.

Biophysical and functional data strongly support the notion that Munc18-1 acts as a template to assemble the neuronal SNARE complex, and that inhibition of this activity underlies diverse forms of regulation of neurotransmitter release.

Neurons of the cholinergic system, which release the excitatory neurotransmitter acetycholine throughout the cortex, also release the inhibitory transmitter GABA, with potential implications for cognitive function.

Long and short variants of a protein called UNC-13, assisted by another called Tomosyn, regulate the timing of synaptic vesicle release in C. elegans.

The mobilization or silencing of two heterogeneous pools of synaptic vesicles via different frequencies probably enables granule cell to Purkinje cell synapses to better discriminate between the high-rate code of sensory information and background noise.