Institut für Neurophysiologie, Charité – Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany
Marta Maglione
Freie Universität Berlin, Institut für Biologie, Berlin, Germany; Leibniz-Forschungsinstitut für Molekulare Pharmakologie (FMP), Berlin, Germany; NeuroCure Cluster of Excellence, Berlin, Germany
Claudia G Willmes
DZNE, German Center for Neurodegenerative Diseases, Berlin, Germany
Alexander Stumpf
Neuroscience Research Center, Charité – Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany
Boris A Bouazza
Institut für Neurophysiologie, Charité – Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany
Laura M Velasquez
Neuroscience Research Center, Charité – Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany
Institut für Neurophysiologie, Charité – Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany
Prateep Beed
Neuroscience Research Center, Charité – Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany
Martin Lehmann
Leibniz-Forschungsinstitut für Molekulare Pharmakologie (FMP), Berlin, Germany
Niclas Gimber
Neuroscience Research Center, Charité – Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany
Freie Universität Berlin, Institut für Biologie, Berlin, Germany; NeuroCure Cluster of Excellence, Berlin, Germany; DZNE, German Center for Neurodegenerative Diseases, Berlin, Germany
Institut für Neurophysiologie, Charité – Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany; NeuroCure Cluster of Excellence, Berlin, Germany
Dietmar Schmitz
NeuroCure Cluster of Excellence, Berlin, Germany; DZNE, German Center for Neurodegenerative Diseases, Berlin, Germany; Neuroscience Research Center, Charité – Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany
All synapses require fusion-competent vesicles and coordinated Ca2+-secretion coupling for neurotransmission, yet functional and anatomical properties are diverse across different synapse types. We show that the presynaptic protein RIM-BP2 has diversified functions in neurotransmitter release at different central murine synapses and thus contributes to synaptic diversity. At hippocampal pyramidal CA3-CA1 synapses, RIM-BP2 loss has a mild effect on neurotransmitter release, by only regulating Ca2+-secretion coupling. However, at hippocampal mossy fiber synapses, RIM-BP2 has a substantial impact on neurotransmitter release by promoting vesicle docking/priming and vesicular release probability via stabilization of Munc13-1 at the active zone. We suggest that differences in the active zone organization may dictate the role a protein plays in synaptic transmission and that differences in active zone architecture is a major determinant factor in the functional diversity of synapses.
