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

First Author  Altrock WD Year  2003
Journal  Neuron Volume  37
Issue  5 Pages  787-800
PubMed ID  12628169 Mgi Jnum  J:82241
Mgi Id  MGI:2651944 Doi  10.1016/s0896-6273(03)00088-6
Citation  Altrock WD, 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
abstractText  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.
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