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.
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.
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.
A combination of advanced optical imaging and cryogenic electron microscopy has been used to explore membrane fusion in a synthetic system and provide new insights into neurotransmitter release.
Ca2+-free synaptotagmin-1 binds to neuronal SNARE complexes anchored on nanodiscs, and Ca2+ releases this interaction to induce tight, specific binding to PIP2-containing membranes.
Inhibition from the cerebellar nuclei to the inferior olive is exclusively asynchronous and GABAergic, whereas the vestibular nuclei provide rapid synchronous inhibition mediated by mixed GABA and glycinergic synapses.
A model for synchronous neurotransmitter release suggests that when not in the presence of calcium ions, Synaptotagmin proteins form ring-like structures between the vesicle and plasma membrane that prevent spontaneous fusion.
Skeletal muscle cells constantly monitor their own activity and that of their partner neuron at synapses, enabling them to provide the neuron with feedback regarding neurotransmitter release.
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.