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      Munc13-1 is essential for fusion competence of glutamatergic synaptic vesicles.

      Nature

      Animals, Cells, Cultured, Dizocilpine Maleate, pharmacology, Excitatory Amino Acid Antagonists, Glutamic Acid, metabolism, Hippocampus, cytology, physiology, Intracellular Signaling Peptides and Proteins, Membrane Fusion, Mice, Nerve Tissue Proteins, genetics, Neurons, ultrastructure, Receptors, N-Methyl-D-Aspartate, antagonists & inhibitors, Sequence Deletion, Spider Venoms, Synapses, Synaptic Transmission, drug effects, Synaptic Vesicles, gamma-Aminobutyric Acid, Action Potentials

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          Abstract

          Neurotransmitter release at synapses between nerve cells is mediated by calcium-triggered exocytotic fusion of synaptic vesicles. Before fusion, vesicles dock at the presynaptic release site where they mature to a fusion-competent state. Here we identify Munc13-1, a brain-specific presynaptic phorbol ester receptor, as an essential protein for synaptic vesicle maturation. We show that glutamatergic hippocampal neurons from mice lacking Munc13-1 form ultrastructurally normal synapses whose synaptic-vesicle cycle is arrested at the maturation step. Transmitter release from mutant synapses cannot be triggered by action potentials, calcium-ionophores or hypertonic sucrose solution. In contrast, release evoked by alpha-latrotoxin is indistinguishable from wild-type controls, indicating that the toxin can bypass Munc13-1-mediated vesicle maturation. A small subpopulation of synapses of any given glutamatergic neuron as well as all synapses of GABA (gamma-aminobutyric acid)-containing neurons are unaffected by Munc13-1 loss, demonstrating the existence of multiple and transmitter-specific synaptic vesicle maturation processes in synapses.

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          Journal
          10440375
          10.1038/22768

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