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Functional Inactivation of a Fraction of Excitatory Synapses in Mice Deficient for the Active Zone Protein Bassoon
Open accessAbstract
Mutant mice lacking the central region of the presynaptic active zone protein Bassoon were generated to establish the role of this protein in the assembly and function of active zones as sites of synaptic vesicle docking and fusion. Our data show that the loss of Bassoon causes a reduction in normal synaptic transmission, which can be attributed to the inactivation of a significant fraction of glutamatergic synapses. At these synapses, vesicles are clustered and docked in normal numbers but are unable to fuse. Phenotypically, the loss of Bassoon causes spontaneous epileptic seizures. These data show that Bassoon is not essential for synapse formation but plays an essential role in the regulated neurotransmitter release from a subset of glutamatergic synapses.
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“Partial knockout of bassoon causes partial lethality and impairs neurotransmitter release (Altrock et al., 2003)”
From The Presynaptic Active Zone (2012) · cites this paper as Altrock et al., 2003
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Metadata
- Authors
- Altrock, W. D., tom Dieck, S., Sokolov, M., Meyer, A. C., Sigler, A., Brakebusch, C., Fässler, R., Richter, K., Boeckers, T. M., Potschka, H., Brandt, C., Löscher, W., Grimberg, D., Dresbach, T., Hempelmann, A., Hassan, H., Balschun, D., Frey, J. U., Brandstätter, J. H., Garner, C. C., Rosenmund, C., & Gundelfinger, E. D.
- Affiliations
- Leibniz Institute for Neurobiology (DE)
- Max Planck Institute for Biophysical Chemistry (DE)
- Max Planck Society (DE)
- Otto-von-Guericke-Universität Magdeburg (DE)
- University of Münster (DE)
- University of Veterinary Medicine Hannover, Foundation (DE)
- Max Planck Institute for Brain Research (DE)
- Stanford University (US)
- Corresponding author
- Gundelfinger, Eckart D.
- ORCID
- Venue
- Neuron
- Publisher
- Elsevier BV
- Published
- 2003-03
- Volume
- 37
- Issue
- 5
- Pages
- 787-800
- ISSN
- 0896-6273 (ISSN-L)
- OpenAlex
- W2091013445
- Cited by
- 258
- References
- 47
- Citations by year
- 2026: 5 · 2025: 5 · 2024: 6 · 2023: 10 · 2022: 11 · 2021: 7 · 2020: 11 · 2019: 8 · 2018: 8 · 2017: 13 · 2016: 9 · 2015: 9 · 2014: 11 · 2013: 14 · 2012: 13
- FWCI
- 5.26
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Neuron (publishedVersion)
- PubMed (publishedVersion)
- Max Planck Institute for Plasma Physics (submittedVersion)
- Research at the University of Copenhagen (University of Copenhagen) (submittedVersion)
- MPG.PuRe (Max Planck Society) (submittedVersion)
- MPG.PuRe (Max Planck Society) (submittedVersion, other-oa)
- Funders
- National Institutes of Health (5p01ag006569-13, 5p50hd032901-05)
- National Institute on Aging (P01 AG06569)
- National Institute of Neurological Disorders and Stroke (R01NS039471, R01-NS39471)
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (P50 HD32901)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Cellular transport and secretion
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
- Keywords
- bassoon, active zone, excitatory synapses, glutamatergic synapses, synaptic vesicle fusion, synaptic vesicle docking, synaptic transmission, synaptogenesis, mouse mutants
- MeSH terms
- Animals, Cells, Cultured, Hippocampus, Male, Mice, Mutant Strains, Mutation, Nerve Tissue Proteins, Neurons, Synapses, Excitatory Postsynaptic Potentials, Gene Silencing, Mice, In Vitro Techniques
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