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

Altrock, W. D.; tom Dieck, S.; 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.

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

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tom Dieck, S.
Synaptic Plasticity Department, Max Planck Institute for Brain Research, Max Planck Society;

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Fässler, R.
Neuroanatomy Department, Max Planck Institute for Brain Research, Max Planck Society;

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Dresbach, T.
Neurochemistry Department, Max Planck Institute for Brain Research, Max Planck Society;

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Brandstätter, J. H.
Neuroanatomy Department, Max Planck Institute for Brain Research, Max Planck Society;

Rosenmund, C.
Max Planck Society;

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Citation

Altrock, W. D., tom Dieck, S., 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-0000-002E-1FCC-4

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.