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Synaptic vesicle endocytosis is the biological process by which the plasma membrane at the pre-synaptic axon terminal invaginates to create membrane-bound synaptic vesicles. This process enables the neuron to recover and recycle the membrane that is added to the plasma membrane during synaptic vesicle exocytosis.
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.
The authors describe the mechanism of exo-endocytosis coupling at synapses. They find that actin forms a ring around the region of exocytosis. This ring conserves membrane area, allowing induction of inward membrane buckling following exocytosis.
Following synaptic vesicle exocytosis, synaptotagmin 1 recruits a lipid signalling pathway within the presynaptic plasma membrane that drives local dynamin recruitment and membrane retrieval by endocytosis, thus maintaining membrane homeostasis.
Dynamin mediates vesicle scission during endocytosis, and here is shown to exist with syndapin 1 in biomolecular condensates at the endocytic zone that enable its participation in ultrafast endocytosis.