Functional inactivation of a fraction of excitatory synapses in mice deficient for the active zone protein bassoon
- Wilko D. Altrock,
- Susanne Tom Dieck,
- Maxim Sokolov,
- Alexander C. Meyer,
- Albrecht Sigler,
- Cord Brakebusch
- Leibniz Institute for Neurobiology,
- Max Planck Institute for Brain Research,
- Max Planck Institute for Biophysical Chemistry (Karl Friedrich Bonhoeffer Institute),
- Max Planck Institute of Biochemistry,
- Otto von Guericke University Magdeburg,
- University of Münster
Open access
Abstract
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.
Publication Information
Output type
Original language
English (US)Pages from-to (Number of pages)
Pages 787-800 (14 pages)Journal (Volume, Issue Number)
Neuron (Volume 37, Issue 5)Publication milestones
- Published - 03/06/2003
Publication status
ISSN
0896-6273Publication IDs
- Scopus: 0037421990
- PubMed: 12628169