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.
authors.affiliation: Leibniz Institute for Neurobiology, 39118 Magdeburg, Germany.
authors.forename: Wilko D
authors.initials: WD
authors.lastname: Altrock
authors.forename: Susanne
authors.initials: S
authors.lastname: tom Dieck
authors.forename: Maxim
authors.initials: M
authors.lastname: Sokolov
authors.forename: Alexander C
authors.initials: AC
authors.lastname: Meyer
authors.forename: Albrecht
authors.initials: A
authors.lastname: Sigler
authors.forename: Cord
authors.initials: C
authors.lastname: Brakebusch
authors.forename: Reinhard
authors.initials: R
authors.lastname: Fässler
authors.forename: Karin
authors.initials: K
authors.lastname: Richter
authors.forename: Tobias M
authors.initials: TM
authors.lastname: Boeckers
authors.forename: Heidrun
authors.initials: H
authors.lastname: Potschka
authors.forename: Claudia
authors.initials: C
authors.lastname: Brandt
authors.forename: Wolfgang
authors.initials: W
authors.lastname: Löscher
authors.forename: Dörte
authors.initials: D
authors.lastname: Grimberg
authors.forename: Thomas
authors.initials: T
authors.lastname: Dresbach
authors.forename: Anne
authors.initials: A
authors.lastname: Hempelmann
authors.forename: Hadir
authors.initials: H
authors.lastname: Hassan
authors.forename: Detlef
authors.initials: D
authors.lastname: Balschun
authors.forename: Julietta U
authors.initials: JU
authors.lastname: Frey
authors.forename: Johann H
authors.initials: JH
authors.lastname: Brandstätter
authors.forename: Craig C
authors.initials: CC
authors.lastname: Garner
authors.forename: Christian
authors.initials: C
authors.lastname: Rosenmund
authors.forename: Eckart D
authors.initials: ED
authors.lastname: Gundelfinger
mesh_terms: 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
chemical_list: C498441:Bsn protein, mouse; D009419:Nerve Tissue Proteins