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.

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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., 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.

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Item Permalink: https://hdl.handle.net/11858/00-001M-0000-002E-1EFE-B Version Permalink: https://hdl.handle.net/11858/00-001M-0000-002E-1EFF-9

Genre: Journal Article

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Creators:
Altrock, W. D., Author
Dieck, S. T.¹, Author
Sokolov, M., Author
Meyer, A. C., Author
Sigler, A., Author
Brakebusch, C.², Author
Fässler, R.³, Author
Richter, K., Author
Boeckers, T. M., Author
Potschka, H., Author
Brandt, C., Author
Loscher, W., Author
Grimberg, D., Author
Dresbach, T.⁴, Author
Hempelmann, A., Author
Hassan, H., Author
Balschun, D., Author
Frey, J. U., Author
Brandstätter, J. H.³, Author
Garner, C. C., Author
Rosenmund, C., AuthorGundelfinger, E. D., Author more..

Affiliations:
1Synaptic Plasticity Department, Max Planck Institute for Brain Research, Max Planck Society, ou_2461710
2Max Planck Society, ou_persistent13
3Neuroanatomy Department, Max Planck Institute for Brain Research, Max Planck Society, ou_2461703
4Neurochemistry Department, Max Planck Institute for Brain Research, Max Planck Society, ou_2461704

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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.

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Language(s): eng - English

Dates: Date issued: 2003-03-06

Publication Status: Issued

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Rev. Type: Peer

Identifiers: eDoc: 41844
ISI: 000181452800008

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Title: Neuron

Alternative Title : Neuron

Source Genre: Journal

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Pages: - Volume / Issue: 37 (5) Sequence Number: - Start / End Page: 787 - 800 Identifier: ISSN: 0896-6273