Previous Article | Next Article 
Molecular and Cellular Biology, September 2001, p. 5970-5978, Vol. 21, No. 17
0270-7306/01/$04.00+0 DOI: 10.1128/MCB.21.17.5970-5978.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
Neurocan Is Dispensable for Brain
Development
Xiao-Hong
Zhou,1
Cord
Brakebusch,1
Henry
Matthies,2
Toshitaka
Oohashi,3
Emilio
Hirsch,3
Markus
Moser,4
Manfred
Krug,2
Constanze I.
Seidenbecher,5
Tobias M.
Boeckers,5,6
Uwe
Rauch,1
Reinhard
Buettner,4
Eckart D.
Gundelfinger,5 and
Reinhard
Fässler1,3,*
Department of Experimental Pathology, Lund
University, 221 85 Lund, Sweden,1 and
Institute for Pharmacology and Toxicology, Otto von
Guericke University, 39120 Magdeburg,2
Max Planck Institute for Biochemistry, 82152 Martinsried,3 Institute of Pathology,
University Hospital of RWTH Aachen, 52074 Aachen,4 Leibniz Institute for
Neurobiology, 39118 Magdeburg,5 and AG
Molecular Neurobiology, Institute for Anatomy, Westfälische
Wilhelms-Universität, 48149 Münster,6 Germany
Received 23 April 2001/Accepted 30 May 2001
Neurocan is a component of the extracellular matrix in brain. Due
to its inhibition of neuronal adhesion and outgrowth in vitro and its
expression pattern in vivo it was suggested to play an important role
in axon guidance and neurite growth. To study the role of neurocan
in brain development we generated neurocan-deficient mice by targeted
disruption of the neurocan gene. These mice are viable and fertile and
have no obvious deficits in reproduction and general performance. Brain
anatomy, morphology, and ultrastructure are similar to those of
wild-type mice. Perineuronal nets surrounding neurons appear largely
normal. Mild deficits in synaptic plasticity may exist, as maintenance
of late-phase hippocampal long-term potentiation is reduced. These data
indicate that neurocan has either a redundant or a more subtle function
in the development of the brain.
*
Corresponding author. Mailing address: Department of
Experimental Pathology, Lund University, 221 85 Lund, Sweden. Phone: 46 46 173400. Fax: 46 46 158202. E-mail:
Reinhard.Fassler{at}pat.lu.se.
Molecular and Cellular Biology, September 2001, p. 5970-5978, Vol. 21, No. 17
0270-7306/01/$04.00+0 DOI: 10.1128/MCB.21.17.5970-5978.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
This article has been cited by other articles:
-
Dours-Zimmermann, M. T., Maurer, K., Rauch, U., Stoffel, W., Fassler, R., Zimmermann, D. R.
(2009). Versican V2 Assembles the Extracellular Matrix Surrounding the Nodes of Ranvier in the CNS. J. Neurosci.
29: 7731-7742
[Abstract]
[Full Text]
-
Quaglia, X., Beggah, A. T., Seidenbecher, C., Zurn, A. D.
(2008). Delayed priming promotes CNS regeneration post-rhizotomy in Neurocan and Brevican-deficient mice. Brain
131: 240-249
[Abstract]
[Full Text]
-
Liu, B. P, Cafferty, W. B.J, Budel, S. O, Strittmatter, S. M
(2006). Extracellular regulators of axonal growth in the adult central nervous system. Phil Trans R Soc B
361: 1593-1610
[Abstract]
[Full Text]
-
Spicer, A. P., Joo, A., Bowling, R. A. Jr.
(2003). A Hyaluronan Binding Link Protein Gene Family Whose Members Are Physically Linked Adjacent to Chrondroitin Sulfate Proteoglycan Core Protein Genes: THE MISSING LINKS. J. Biol. Chem.
278: 21083-21091
[Abstract]
[Full Text]
-
Zhang, Y., Rauch, U., Perez, M.-T. R.
(2003). Accumulation of Neurocan, a Brain Chondroitin Sulfate Proteoglycan, in Association with the Retinal Vasculature in RCS Rats. IOVS
44: 1252-1261
[Abstract]
[Full Text]
-
Franken, S., Junghans, U., Rosslenbroich, V., Baader, S. L., Hoffmann, R., Gieselmann, V., Viebahn, C., Kappler, J.
(2003). Collapsin Response Mediator Proteins of Neonatal Rat Brain Interact with Chondroitin Sulfate. J. Biol. Chem.
278: 3241-3250
[Abstract]
[Full Text]
-
Brakebusch, C., Seidenbecher, C. I., Asztely, F., Rauch, U., Matthies, H., Meyer, H., Krug, M., Bockers, T. M., Zhou, X., Kreutz, M. R., Montag, D., Gundelfinger, E. D., Fassler, R.
(2002). Brevican-Deficient Mice Display Impaired Hippocampal CA1 Long-Term Potentiation but Show No Obvious Deficits in Learning and Memory. Mol. Cell. Biol.
22: 7417-7427
[Abstract]
[Full Text]
-
Evers, M. R., Salmen, B., Bukalo, O., Rollenhagen, A., Bosl, M. R., Morellini, F., Bartsch, U., Dityatev, A., Schachner, M.
(2002). Impairment of L-type Ca2+ Channel-Dependent Forms of Hippocampal Synaptic Plasticity in Mice Deficient in the Extracellular Matrix Glycoprotein Tenascin-C. J. Neurosci.
22: 7177-7194
[Abstract]
[Full Text]