Functional inactivation of a fraction of excitatory synapses in mice deficient 
for the active zone protein bassoon

Altrock, W. D.; Dieck, S. T.; Sokolov, M.; Meyer, A. C.; Sigler, A.; Brakebusch, C.; Fässler, R.; Richter, K.; Boeckers, T. M.; Potschka, H.; Brandt, C.; Loscher, 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.

Item

ITEM ACTIONSEXPORT

Add to Basket

Local TagsRelease HistoryDetailsSummary

Released

Journal Article

Functional inactivation of a fraction of excitatory synapses in mice deficient for the active zone protein bassoon

MPS-Authors

/persons/resource/persons77799

Brakebusch, C.
Former Research Groups, Max Planck Institute of Biochemistry, Max Planck Society;

/persons/resource/persons77945

Fässler, R.
Fässler, Reinhard / Molecular Medicine, Max Planck Institute of Biochemistry, Max Planck Society;

External Resource

No external resources are shared

Fulltext (restricted access)

There are currently no full texts shared for your IP range.

Fulltext (public)

There are no public fulltexts stored in PuRe

Supplementary Material (public)

There is no public supplementary material available

Citation

Altrock, W. D., Dieck, S. T., Sokolov, M., Meyer, A. C., Sigler, A., Brakebusch, C., et al. (2003). Functional inactivation of a fraction of excitatory synapses in mice deficient for the active zone protein bassoon. Neuron, 37(5), 787-800.

Cite as: https://hdl.handle.net/11858/00-001M-0000-0010-6C7B-E

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.