Brevican-deficient mice display impaired hippocampal CA1 long-term potentiation but show no obvious deficits in learning and memory

被引:196
作者
Brakebusch, C
Seidenbecher, CI
Asztely, F
Rauch, U
Matthies, H
Meyer, H
Krug, M
Böckers, TM
Zhou, XH
Kreutz, MR
Montag, D
Gundelfinger, ED
Fässler, R
机构
[1] Max Planck Inst Biochem, Dept Mol Med, D-82152 Martinsried, Germany
[2] Leibniz Inst Neurobiol, Dept Neurochem & Mol Biol, D-39118 Magdeburg, Germany
[3] Leibniz Inst Neurobiol, Neurogenet Res Grp, D-39118 Magdeburg, Germany
[4] Univ Munster, Inst Anat, D-48149 Munster, Germany
[5] Univ Lund Hosp, Dept Expt Pathol, S-22185 Lund, Sweden
[6] Univ Lund Hosp, Dept Neurol, S-22185 Lund, Sweden
关键词
D O I
10.1128/MCB.22.21.7417-7427.2002
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Brevican is a brain-specific proteoglycan which is found in specialized extracellular matrix structures called perineuronal nets. Brevican increases the invasiveness of glioma cells in vivo and has been suggested to play a role in central nervous system fiber tract development. To study the role of brevican in the development and function of the brain, we generated mice lacking a functional brevican gene. These mice are viable and fertile and have a normal life span. Brain anatomy was normal, although alterations in the expression of neurocan were detected. Perineuronal nets formed but appeared to be less prominent in mutant than in wild-type mice. Brevican-deficient mice showed significant deficits in the maintenance of hippocampal long-term potentiation (LTP). However, no obvious impairment of excitatory and inhibitory synaptic transmission was found, suggesting a complex cause for the LTP defect. Detailed behavioral analysis revealed no statistically significant deficits in learning and memory. These data indicate that brevican is not crucial for brain development but has restricted structural and functional roles.
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收藏
页码:7417 / 7427
页数:11
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