Ca²⁺ channels and release sensors at a fast central synapse are tightly coupled, which minimizes the effect of extracellular Ca²⁺ concentration on the timing of transmitter release.

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.

A naturally occurring intracellular peptide, derived by processing the Alzheimer's protein APP, reduces synaptic transmission by acting as a dominant negative of APP.

Deep penetration and transmission of mechanical force to regulate ER functions depends on not only the passive cytoskeletal support, but also the active actomyosin contractility, which is dispensable for mechanotransduction at the plasma membrane.

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.

Cells within the retina synchronize transmitter release across their output synapses in the dark, reducing the impact of noise generated at these synapses and allowing light-dependent signals to be transmitted with minimal added synaptic noise.

The molecular mechanisms by which midbrain dopamine neurons acquire the inhibitory neurotransmitter GABA for synaptic release are revealed.

A combination of tethered diffusion of release-ready synaptic vesicles and vesicle-vesicle fusion supports neurotransmitter release at the presynaptic active zone of sensory synapses.

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.

A surface protein triggers intra-oocyst motility of Plasmodium sporozoites to ensure parasite egress from oocysts.