Molecular and Cellular Biology, November 2002, p. 7417-7427, Vol. 22, No. 21
0270-7306/02/$04.00+0 DOI: 10.1128/MCB.22.21.7417-7427.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.
Brevican-Deficient Mice Display Impaired Hippocampal CA1 Long-Term Potentiation but Show No Obvious Deficits in Learning and Memory
Cord Brakebusch,1,2 Constanze I. Seidenbecher,3 Fredrik Asztely,4 Uwe Rauch,2 Henry Matthies,3 Hannelore Meyer,1 Manfred Krug,3 Tobias M. Böckers,5 Xiaohong Zhou,2 Michael R. Kreutz,3 Dirk Montag,6 Eckart D. Gundelfinger,3 and Reinhard Fässler1,2*
Department of Molecular Medicine, Max Planck Institute of Biochemistry, 82152 Martinsried,1
Department of Neurochemistry and Molecular Biology,3
Neurogenetics Research Group, Leibniz Institute for Neurobiology, 39118 Magdeburg,6
Institute for Anatomy, University of Münster, 48149 Münster, Germany,5
Department of Experimental Pathology,2
Department of Neurology, Lund University Hospital, 22185 Lund, Sweden4
Received 17 April 2002/
Returned for modification 10 June 2002/
Accepted 16 July 2002
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.
* Corresponding author. Mailing address: Department of Molecular Medicine, Max Planck Institute of Biochemistry, Am Klopferspitz 18A, 82152 Martinsried, Germany. Phone.: 49-89-8578 2897. Fax: 49-89-8578 2422. E-mail: faessler{at}biochem.mpg.de.
Molecular and Cellular Biology, November 2002, p. 7417-7427, Vol. 22, No. 21
0022-538X/02/$04.00+0 DOI: 10.1128/MCB.22.21.7417-7427.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.
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Copyright © 2002 by the American Society for Microbiology. All rights reserved.