| Literature DB >> 12628169 |
Wilko D Altrock1, 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 Garner, Christian Rosenmund, Eckart D Gundelfinger.
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.Entities:
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Year: 2003 PMID： 12628169 DOI： 10.1016/s0896-6273(03)00088-6
Source DB: PubMed Journal: Neuron ISSN： 0896-6273 Impact factor: 17.173