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The priming protein ubMunc13-2 and Synaptotagmin-7 cooperate with phorbolesters/diacylglycerol to stimulate vesicle priming in adrenal chromaffin cells, whereas phorbolesters/diacylglycerol interacting with Munc13-1 inhibit vesicle fusion, which identifies opposing functions of these two Munc13 proteins.

A technology for measuring release of dopamine simultaneously from hundreds of release sites at the spatial resolution of a synapse is provided.

Lactic acid bacteria engage a hybrid metabolism which blends features of fermentation and respiration when they perform extracellular electron transfer.

Electrophysiological and live-cell imaging analyses identify a presynaptic function of Ca²⁺ influx via transient receptor potential melastatin 7 (TRPM7) channels.

During neurotransmitter release, calcium-induced membrane insertion of the C2B domain of Synaptotagmin re-orients the bound SNARE complex which dilates the fusion pore in a mechanical lever action.

A dopamine transporter deficiency syndrome (DTDS)-linked mutation, R445C, underlies dopamine dysfunction and, more broadly, the clinical phenotypes shared by DTDS and Parkinson’s disease.

Synaptotagmin-7 acts synergistically with synaptotagmin-1 by placing vesicles close to the plasma membrane within reach of the SNARE/Munc13-complex, supporting their priming and setting the stage for fast and slow fusion.

Fast fluctuations of oxygen, linked to behavioral and neural dynamics in vivo, cause phasic transients is amperometry-measured cholinergic signals via the mechanism of non-steady-state enzyme kinetics in the choline-oxidase-based biosensor.

Extensive mass spectrometry-based profiling of polar metabolites within synaptic vesicles that are rapidly isolated either from cultured mouse neurons or directly from mouse brains reveals their neurotransmitter composition.

Genetic and electrophysiological analyses reveal calcium-triggering mechanisms for dopamine release in the striatum that may enable fast and slow dopamine coding.