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Cited by 223Neuroscience and Neuropharmacology ResearchCellular transport and secretionGenetics and Neurodevelopmental Disorders

Bassoon speeds vesicle reloading at a central excitatory synapse

Open access
Hallermann, Stefan, Fejtova, Anna, Schmidt, Hartmut, Weyhersmüller, Annika, Silver, R. Angus, Gundelfinger, Eckart D., Eilers, Jens·2010·Neuron
DOI 10.1016/j.neuron.2010.10.026PMC PMC3004039
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Abstract

Sustained rate-coded signals encode many types of sensory modalities. Some sensory synapses possess specialized ribbon structures, which tether vesicles, to enable high-frequency signaling. However, central synapses lack these structures, yet some can maintain signaling over a wide bandwidth. To analyze the underlying molecular mechanisms, we investigated the function of the active zone core component Bassoon in cerebellar mossy fiber to granule cell synapses. We show that short-term synaptic depression is enhanced in Bassoon knockout mice during sustained high-frequency trains but basal synaptic transmission is unaffected. Fluctuation and quantal analysis as well as quantification with constrained short-term plasticity models revealed that the vesicle reloading rate was halved in the absence of Bassoon. Thus, our data show that the cytomatrix protein Bassoon speeds the reloading of vesicles to release sites at a central excitatory synapse.

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Crossref · 10.1016/j.neuron.2010.10.026

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  • Piccolo and bassoon are large proteins specific to vertebrates whose major function appears to be to guide synaptic vesicles from the backfield of the synapse to the active zone.

    “Piccolo and bassoon are large proteins specific to vertebrates whose major function appears to be to guide synaptic vesicles from the backfield of the synapse to the active zone (Mukherjee et al., 2010; Hallermann et al., 2010).”

    From The Presynaptic Active Zone (2012) · cites this paper as Hallermann et al., 2010

    The Introduction describes Bassoon as very large and says Bassoon and Piccolo appear to be vertebrate-specific. The Discussion and Abstract support a role for Bassoon in vesicle supply and reloading, and the Discussion reports impaired vesicle clustering in Bassoon–Piccolo double knockouts. They do not establish that guiding vesicles from the synaptic backfield to the active zone is the major function of both proteins. (LLM, conf=0.86)

    Experimental — accuracy not yet measured

  • A deletion of the 17 C-terminal residues of bruchpilot impaired attachment of synaptic vesicles to t bars in Drosophila synapses and altered synaptic transmission.

    “a deletion of the 17 C-terminal residues of bruchpilot (which are part of the plectin-homology region) impaired attachment of synaptic vesicles to t bars in Drosophila synapses and altered synaptic transmission”

    From The Presynaptic Active Zone (2012) · cites this paper as Hallermann et al., 2010

    The Results discuss Bassoon-deficient mouse synapses, and the Discussion addresses vesicle tethering by Bassoon, not bruchpilot at Drosophila t bars. Searches for bruchpilot, the 17 C-terminal residues, and the plectin-homology region found no passage in our copy addressing the claimed deletion or its effects. (LLM, conf=0.76)

    Experimental — accuracy not yet measured

  • A major contribution to bruchpilot function is derived from the plectin-homology region.

    “suggesting that a major contribution to bruchpilot function is derived from the plectin-homology region (Hallermann et al., 2010).”

    From The Presynaptic Active Zone (2012) · cites this paper as Hallermann et al., 2010

    The Introduction and Discussion address Bassoon’s role at synaptic active zones, not Bruchpilot’s functional regions. Searches of our copy for “Bruchpilot,” “plectin,” and “plectin-homology region” found no passage addressing the attributed claim; page numbers were not available. (LLM, conf=0.76)

    Experimental — accuracy not yet measured

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Authors
Hallermann, S., Fejtova, A., Schmidt, H., Weyhersmüller, A., Silver, R. A., Gundelfinger, E. D., & Eilers, J.
Affiliations
  • Leipzig University (DE)
  • University College London (GB)
  • Leibniz Institute for Neurobiology (DE)
Corresponding author
Hallermann, Stefan
ORCID
Venue
Neuron
Publisher
Elsevier BV
Published
2010-11
Volume
68
Issue
4
Pages
710-723
ISSN
0896-6273 (ISSN-L)
DOI
10.1016/j.neuron.2010.10.026
PMC
PMC3004039
OpenAlex
W2050878615
Cited by
223
References
67
Citations by year
2026: 7 · 2025: 13 · 2024: 7 · 2023: 12 · 2022: 15 · 2021: 11 · 2020: 16 · 2019: 17 · 2018: 13 · 2017: 16 · 2016: 17 · 2015: 13 · 2014: 17 · 2013: 15 · 2012: 16
FWCI
6.34
Type
journal article
Language
en
Open access
Licence
Locations
  • Neuron (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • UCL Discovery (University College London) (submittedVersion)
Funders
Wellcome Trust
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, short-term synaptic depression, cerebellum, active zone, quantal analysis, rate coding
MeSH terms
Animals, Cells, Cultured, Cerebellum, Hippocampus, Mice, Inbred C57BL, Mice, Transgenic, Nerve Tissue Proteins, Neural Inhibition, Reaction Time, Synapses, Synaptic Vesicles, Time Factors, Mice, Knockout, Excitatory Postsynaptic Potentials, Mice, Mice, 129 Strain

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