Functional inactivation of a fraction of excitatory synapses in mice deficient for the active zone protein bassoon.
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.
Altrock
Wilko D
WD
Leibniz Institute for Neurobiology, 39118 Magdeburg, Germany.
tom Dieck
Susanne
S
Sokolov
Maxim
M
Meyer
Alexander C
AC
Sigler
Albrecht
A
Brakebusch
Cord
C
Fässler
Reinhard
R
Richter
Karin
K
Boeckers
Tobias M
TM
Potschka
Heidrun
H
Brandt
Claudia
C
Löscher
Wolfgang
W
Grimberg
Dörte
D
Dresbach
Thomas
T
Hempelmann
Anne
A
Hassan
Hadir
H
Balschun
Detlef
D
Frey
Julietta U
JU
Brandstätter
Johann H
JH
Garner
Craig C
CC
Rosenmund
Christian
C
Gundelfinger
Eckart D
ED
D000818:Animals; D002478:Cells, Cultured; D019706:Excitatory Postsynaptic Potentials / Q000502:physiology*; D020868:Gene Silencing / Q000502:physiology*; D006624:Hippocampus / Q000166:cytology / Q000502:physiology / Q000648:ultrastructure; D066298:In Vitro Techniques; D008297:Male; D051379:Mice; D008817:Mice, Mutant Strains; D009154:Mutation; D009419:Nerve Tissue Proteins / Q000096:biosynthesis / Q000172:deficiency* / Q000235:genetics / Q000502:physiology*; D009474:Neurons / Q000166:cytology / Q000502:physiology / Q000648:ultrastructure; D013569:Synapses / Q000502:physiology* / Q000648:ultrastructure
C498441:Bsn protein, mouse; D009419:Nerve Tissue Proteins