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

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Standard

Functional inactivation of a fraction of excitatory synapses in mice deficient for the active zone protein bassoon. / Altrock, Wilko D; tom Dieck, Susanne; Sokolov, Maxim; Meyer, Alexander C; Sigler, Albrecht; Brakebusch, Cord; Fässler, Reinhard; Richter, Karin; Boeckers, Tobias M; Potschka, Heidrun; Brandt, Claudia; Löscher, Wolfgang; Grimberg, Dörte; Dresbach, Thomas; Hempelmann, Anne; Hassan, Hadir; Balschun, Detlef; Frey, Julietta U; Brandstätter, Johann H; Garner, Craig C; Rosenmund, Christian; Gundelfinger, Eckart D.

I: Neuron, Bind 37, Nr. 5, 2003, s. 787-800.

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt

Harvard

Altrock, WD, tom Dieck, S, Sokolov, M, Meyer, AC, Sigler, A, Brakebusch, C, Fässler, R, Richter, K, Boeckers, TM, Potschka, H, Brandt, C, Löscher, W, Grimberg, D, Dresbach, T, Hempelmann, A, Hassan, H, Balschun, D, Frey, JU, Brandstätter, JH, Garner, CC, Rosenmund, C & Gundelfinger, ED 2003, 'Functional inactivation of a fraction of excitatory synapses in mice deficient for the active zone protein bassoon.', Neuron, bind 37, nr. 5, s. 787-800.

APA

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., Löscher, W., Grimberg, D., Dresbach, T., Hempelmann, A., Hassan, H., Balschun, D., Frey, J. U., Brandstätter, J. H., ... Gundelfinger, E. D. (2003). Functional inactivation of a fraction of excitatory synapses in mice deficient for the active zone protein bassoon. Neuron, 37(5), 787-800.

Vancouver

Altrock WD, tom Dieck S, Sokolov M, Meyer AC, Sigler A, Brakebusch C o.a. Functional inactivation of a fraction of excitatory synapses in mice deficient for the active zone protein bassoon. Neuron. 2003;37(5):787-800.

Author

Altrock, Wilko D ; tom Dieck, Susanne ; Sokolov, Maxim ; Meyer, Alexander C ; Sigler, Albrecht ; Brakebusch, Cord ; Fässler, Reinhard ; Richter, Karin ; Boeckers, Tobias M ; Potschka, Heidrun ; Brandt, Claudia ; Löscher, Wolfgang ; Grimberg, Dörte ; Dresbach, Thomas ; Hempelmann, Anne ; Hassan, Hadir ; Balschun, Detlef ; Frey, Julietta U ; Brandstätter, Johann H ; Garner, Craig C ; Rosenmund, Christian ; Gundelfinger, Eckart D. / Functional inactivation of a fraction of excitatory synapses in mice deficient for the active zone protein bassoon. I: Neuron. 2003 ; Bind 37, Nr. 5. s. 787-800.

Bibtex

@article{cf081e10589511dd8d9f000ea68e967b,
title = "Functional inactivation of a fraction of excitatory synapses in mice deficient for the active zone protein bassoon.",
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.",
author = "Altrock, {Wilko D} and {tom Dieck}, Susanne and Maxim Sokolov and Meyer, {Alexander C} and Albrecht Sigler and Cord Brakebusch and Reinhard F{\"a}ssler and Karin Richter and Boeckers, {Tobias M} and Heidrun Potschka and Claudia Brandt and Wolfgang L{\"o}scher and D{\"o}rte Grimberg and Thomas Dresbach and Anne Hempelmann and Hadir Hassan and Detlef Balschun and Frey, {Julietta U} and Brandst{\"a}tter, {Johann H} and Garner, {Craig C} and Christian Rosenmund and Gundelfinger, {Eckart D}",
note = "Keywords: Animals; Cells, Cultured; Excitatory Postsynaptic Potentials; Gene Silencing; Hippocampus; Male; Mice; Mice, Mutant Strains; Mutation; Nerve Tissue Proteins; Neurons; Synapses",
year = "2003",
language = "English",
volume = "37",
pages = "787--800",
journal = "Neuron",
issn = "0896-6273",
publisher = "Cell Press",
number = "5",

}

RIS

TY - JOUR

T1 - Functional inactivation of a fraction of excitatory synapses in mice deficient for the active zone protein bassoon.

AU - Altrock, Wilko D

AU - tom Dieck, Susanne

AU - Sokolov, Maxim

AU - Meyer, Alexander C

AU - Sigler, Albrecht

AU - Brakebusch, Cord

AU - Fässler, Reinhard

AU - Richter, Karin

AU - Boeckers, Tobias M

AU - Potschka, Heidrun

AU - Brandt, Claudia

AU - Löscher, Wolfgang

AU - Grimberg, Dörte

AU - Dresbach, Thomas

AU - Hempelmann, Anne

AU - Hassan, Hadir

AU - Balschun, Detlef

AU - Frey, Julietta U

AU - Brandstätter, Johann H

AU - Garner, Craig C

AU - Rosenmund, Christian

AU - Gundelfinger, Eckart D

N1 - Keywords: Animals; Cells, Cultured; Excitatory Postsynaptic Potentials; Gene Silencing; Hippocampus; Male; Mice; Mice, Mutant Strains; Mutation; Nerve Tissue Proteins; Neurons; Synapses

PY - 2003

Y1 - 2003

N2 - 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.

AB - 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.

M3 - Journal article

C2 - 12628169

VL - 37

SP - 787

EP - 800

JO - Neuron

JF - Neuron

SN - 0896-6273

IS - 5

ER -

ID: 5141375