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 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.

Targeting Abelson kinase can be beneficial for treating disorders characterized by dysregulated Down Syndrome Cell Adhesion Molecule signaling.

Genetic and electrophysiological analyses reveal that the mechanisms orchestrating the induction and expression of homeostatic plasticity are compartmentalized and operate with exquisite specificity on both sides of the synapse.

Oligodendrocytes are actively engaged in the precise control of synaptic functions in the CNS through activity-dependent BDNF signaling.

By combining direct presynaptic patch-clamp electrophysiology and super-resolution microscopy, it was found that KO of RIM-BP2 reduced calcium channel abundance in hippocampal mossy terminals.

Feedback signaling between the synapse and nucleus via FGF22 and IGF2 directs the activity-dependent stabilization of presynaptic terminals in the mouse hippocampus.

Stationary dense-core vesicles depend on the CAPS-1 protein to fuse with the presynaptic membrane.

The subcellular activity of presynaptic terminals of dopamine neurons shapes the reward magnitude and memory specificity.

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