A5086849150- Neuroscience and Neuropharmacology Research
- Cellular transport and secretion
- Lipid Membrane Structure and Behavior
- Photoreceptor and optogenetics research
- Retinal Development and Disorders
- Ion channel regulation and function
- Genetics and Neurodevelopmental Disorders
- Ubiquitin and proteasome pathways
- Receptor Mechanisms and Signaling
- Autism Spectrum Disorder Research
- Mitochondrial Function and Pathology
- Neurogenesis and neuroplasticity mechanisms
- Pancreatic function and diabetes
- Neurobiology and Insect Physiology Research
- Erythrocyte Function and Pathophysiology
- Genetic Neurodegenerative Diseases
- Neuroscience and Neural Engineering
- Neural dynamics and brain function
- Neuroinflammation and Neurodegeneration Mechanisms
- Endoplasmic Reticulum Stress and Disease
- Hearing, Cochlea, Tinnitus, Genetics
- Genetics, Aging, and Longevity in Model Organisms
- Alzheimer's disease research and treatments
- Advanced Fluorescence Microscopy Techniques
- Calcium signaling and nucleotide metabolism
Max Planck Institute for Multidisciplinary Sciences
2022-2025
Children's Hospital of Zhejiang University
2025
Max Planck Institute of Experimental Medicine
2015-2024
Nanoscale Microscopy and Molecular Physiology of the Brain Cluster of Excellence 171 — DFG Research Center 103
2009-2024
University of Göttingen
2015-2024
Multiscale Bioimaging
2021-2024
Max Planck Society
2007-2017
Deutsche Forschungsgemeinschaft
2003-2011
Kobe University
2010
Biologie Labor
2008
Neurons release neurotransmitters by calcium-dependent exocytosis of synaptic vesicles. However, the molecular steps transducing calcium signal into membrane fusion are still an enigma. It is reported here that synaptotagmin, a highly conserved vesicle protein, binds at physiological concentrations in complex with negatively charged phospholipids. This binding specific for and involves cytoplasmic domain synaptotagmin. Calcium dependent on intact oligomeric structure synaptotagmin (it...
At the synapse, presynaptic membranes specialized for vesicular traffic are linked to postsynaptic signal transduction. The mechanisms that connect pre- and into synaptic junctions unknown. Neuroligins beta-neurexins neuronal cell-surface proteins bind each other form asymmetric intercellular junctions. To test whether neuroligin/beta-neurexin junction is related synapses, we generated characterized monoclonal antibodies neuroligin 1. With these antibodies, show 1 synaptic. localization,...
Synaptic vesicles must be primed to fusion competence before they can fuse with the plasma membrane in response increased intracellular Ca 2+ levels. The presynaptic active zone protein Munc13-1 is essential for priming of glutamatergic synaptic hippocampal neurons. However, a small subpopulation synapses any given nerve cell as well all γ-aminobutyratergic (GABAergic) are largely independent Munc13-1. We show here that Munc13-2, only Munc13 isoform coexpressed hippocampus, responsible...
Autism spectrum conditions (ASCs) are heritable characterized by impaired reciprocal social interactions, deficits in language acquisition, and repetitive restricted behaviors interests. In addition to more complex genetic susceptibilities, even mutation of a single gene can lead ASC. Several such monogenic ASC forms caused loss-of-function mutations genes encoding regulators synapse function neurons, including NLGN4. We report that mice with the murine NLGN4 ortholog Nlgn4, which encodes...
Quantal neurotransmitter release at excitatory synapses depends on glutamate import into synaptic vesicles by vesicular transporters (VGLUTs). Of the three known transporters, VGLUT1 and VGLUT2 are expressed prominently in adult brain, but during first two weeks of postnatal development, expression predominates. Targeted deletion mice causes lethality third week. Glutamatergic neurotransmission is drastically reduced neurons from VGLUT1-deficient mice, with a specific reduction quantal size....
Autism spectrum disorder (ASD) is a frequent neurodevelopmental characterized by variable clinical severity. Core symptoms are qualitatively impaired communication and social behavior, highly restricted interests repetitive behaviors. Although recent work on genetic mutations in ASD has shed light the pathophysiology of disease, classifying it essentially as synaptopathy, no treatments available to date. To develop test novel treatment approaches, validated informative animal models...
Synaptotagmin (p65) is an abundant and evolutionarily conserved protein of synaptic vesicles that contains two copies internal repeat homologous to the regulatory region kinase C. In current study, we have investigated biochemical properties synaptotagmin, demonstrating it five domains: intravesicular amino-terminal domain glycosylated but lacks a cleavable signal sequence; single transmembrane region; sequence separating from repeats C; C-homologous repeats; carboxyl-terminal following...
“Spontaneous” Release Trigger Synaptic vesicle release occurs in different phases that can be tightly coupled to action potentials (synchronous), immediately following (asynchronous), or as stochastic events not triggered by (spontaneous). The protein synaptotagmin is thought act the Ca 2+ sensor synchronous phase, but for other two phases, sensors have been identified. Groffen et al. (p. 1614 , published online 11 February) now show cytoplasmic proteins known Doc2 (double C2 domain) are...