Author
Listed:
- Iris Augustin
(Max-Planck-Institut für Experimentelle Medizin, AG Molekulare Neurobiologie)
- Christian Rosenmund
(Max-Planck-Institut fr Biophysikalische Chemie)
- Thomas C. Südhof
(Center for Basic Neuroscience, Howard Hughes Medical Institute, University of Texas Southwestern Medical Center)
- Nils Brose
(Max-Planck-Institut für Experimentelle Medizin, AG Molekulare Neurobiologie)
Abstract
Neurotransmitter release at synapses between nerve cells is mediated by calcium-triggered exocytotic fusion of synaptic vesicles1. Before fusion, vesicles dock at the presynaptic release site where they mature to a fusion-competent state1,2. Here we identify Munc13-1, a brain-specific presynaptic phorbol ester receptor3,4, 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 α-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 (γ-aminobutyric acid)-containing neurons are unaffected by Munc13-1 loss, demonstrating the existence of multiple and transmitter-specific synaptic vesicle maturation processes in synapses.
Suggested Citation
Iris Augustin & Christian Rosenmund & Thomas C. Südhof & Nils Brose, 1999.
"Munc13-1 is essential for fusion competence of glutamatergic synaptic vesicles,"
Nature, Nature, vol. 400(6743), pages 457-461, July.
Handle:
RePEc:nat:nature:v:400:y:1999:i:6743:d:10.1038_22768
DOI: 10.1038/22768
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