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, Reinhard Fässler, Karin Richter, Tobias M. Boeckers, Heidrun Potschka, Claudia Brandt, Wolfgang Löscher, Dörte Grimberg, Thomas Dresbach, Anne Hempelmann, Hadir Hassan, Detlef Balschun, Julietta U. Frey, Johann H. Brandstätter, Craig C. GarnerChristian Rosenmund, Eckart D. Gundelfinger

Research output: Contribution to journalArticlepeer-review

174 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)787-800
Number of pages14
JournalNeuron
Volume37
Issue number5
DOIs
StatePublished - Mar 6 2003

ASJC Scopus subject areas

  • Neuroscience(all)

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