Vesicle trafficking articles from across Nature Portfolio

How synaptic vesicles (SVs) are clustered at the presynapse is suggestive of anchoring processes counteracting their diffusion. Here, the authors co-track recycling and reserve SVs in live neurons to find that Synapsin 2a tetramerization dynamically immobilizes reserve SVs at the presynapse.

Using single-molecule super-resolution microscopy, researchers revealed that Tau controls the recycling pool of synaptic vesicles in hippocampal neurons by forming nanoscale biomolecular condensates that are dynamically regulated by neuronal activity.

One third of all epilepsies are treatment-resistant. Here, the authors show in a genetic model of epilepsy that a repurposed drug can correct cell defects, brain circuits and seizure-like events by accelerating endocytosis.

Synaptotagmin-3 is identified as the presynaptic high-affinity calcium sensor to rapidly replenish synaptic vesicles to maintain steady synaptic transmission.

Synapses are surrounded by an extracellular matrix (ECM) of extremely long-lived proteins that is thought to only be remodeled by proteolysis and de novo synthesis. Here, the authors show an alternative molecular recycling mechanism that occurs for the key ECM protein Tenascin-R.

Two recent papers reveal that the activity-regulated cytoskeleton-associated proteins ARC andDrosophila melanogasterdArc1 auto-assemble into mRNA-containing, virus-like capsids that are released by neurons in exosomal vesicles and that can be endocytosed at the postsynaptic compartment.

A new study has proposed a mechanism for the pathogenesis of cerebral cavernous malformation (CCM) that links endothelial CCM3 deficiency to increased secretion of the vascular destabilizing protein angiopoietin-2 (ANGPT2).