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

被引：184

作者：

Altrock, WD

Dieck, ST

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 ^{[1
]}

Rosenmund, C

Gundelfinger, ED

机构：

[1] Leibniz Inst Neurobiol, D-39118 Magdeburg, Germany

[2] Max Planck Inst Brain Res, Dept Neuroanat, D-60528 Frankfurt, Germany

[3] Max Planck Inst Biophys Chem, Dept Membrane Biophys, D-37070 Gottingen, Germany

[4] Max Planck Inst Biochem, Dept Mol Med, D-82152 Martinsried, Germany

[5] Otto Von Guericke Univ, Inst Med Neurobiol, D-39120 Magdeburg, Germany

[6] Univ Munster, Inst Anat, D-48149 Munster, Germany

[7] Hannover Sch Vet Med, Dept Pharmacol Toxicol & Pharm, D-30559 Hannover, Germany

[8] Stanford Univ, Dept Psychiat & Behav Sci, Palo Alto, CA 94304 USA

来源：

NEURON | 2003年 / 37卷 / 05期

关键词：

D O I：

10.1016/S0896-6273(03)00088-6

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

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.

引用

页码：787 / 800

页数：14

共 44 条

[1] Munc13-1 is essential for fusion competence of glutamatergic synoptic vesicles [J].