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