 |
 Previous Article | Next Article 
Journal of Neuroscience, Vol 15, 1971-1983, Copyright © 1995 by Society for Neuroscience
Tenascin knockout mice: barrels, boundary molecules, and glial scars
DA Steindler, D Settles, HP Erickson, ED Laywell, A Yoshiki, A Faissner and M Kusakabe
Department of Anatomy and Neurobiology, University of Tennessee, Memphis.
In light of a previous report suggesting that the brains of tenascin-
deficient animals are grossly normal, we have studied the somatosensory
cortical barrel field and injured cerebral cortex in postnatal homozygous
tenascin knockout, heterozygote, and normal wild-type mice. Nissl staining,
cytochrome oxidase, and Dil axonal tracing of thalamocortical axonal
projections to the somatosensory cortex, all reveal the formation of normal
barrels in the first postnatal week in homozygous knockout mice that cannot
be distinguished from heterozygote or normal wild-type barrels. In addition
to confirming the absence of tenascin in knockout animals, and reporting
apparently reduced levels of the glycoprotein in barrel boundaries of
heterozygote animals using well-characterized antibodies and
immunocytochemistry, we also studied the DSD-1-PG proteoglycan, another
developmentally regulated molecule known to be associated with transient
glial/glycoconjugate boundaries that surround developing barrels; DSD-1-PG
was also found to be expressed in barrel boundaries in apparently normal
time frames in tenascin knockout mice. Peanut agglutinin (PNA) binding of
galactosyl- containing glycoconjugates also revealed barrel boundaries in
all three genotypes. We also examined the expression of tenascin-R, a
paralog of tenascin-C (referred to here simply as tenascin). As previously
reported, tenascin-R is prominently expressed in subcortical white matter,
and we found it was not expressed in the barrel boundaries in any of the
genotypes. Thus, the absence of tenascin does not result in a compensatory
expression of tenascin-R in the barrel boundaries. Finally, we studied
wounds of the cerebral cortex in the late postnatal mouse. The astroglial
scar formed, for the most part, in the same time course and spatial
distribution in the wild-type and tenascin knockout mice. However, there
may be some differences in the extent of gliosis between the knockout and
the wild type that warrant further study. Roles for boundary molecules like
tenascin during brain pattern formation and injury are reconsidered in
light of these findings on barrel development and cortical lesions in
tenascin-deficient mice.
This article has been cited by other articles:
|
|
|
|
 
C. Giaume, M. Maravall, E. Welker, and G. Bonvento
The Barrel Cortex as a Model to Study Dynamic Neuroglial Interaction
Neuroscientist,
August 1, 2009;
15(4):
351 - 366.
[Abstract]
[PDF]
|
|
|
|
|
|
|
I. Kazanis, A. Belhadi, A. Faissner, and C. ffrench-Constant
The Adult Mouse Subependymal Zone Regenerates Efficiently in the Absence of Tenascin-C
J. Neurosci.,
December 19, 2007;
27(51):
13991 - 13996.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
A. K. Goetz, B. Scheffler, H.-X. Chen, S. Wang, O. Suslov, H. Xiang, O. Brustle, S. N. Roper, and D. A. Steindler
Temporally restricted substrate interactions direct fate and specification of neural precursors derived from embryonic stem cells
PNAS,
July 18, 2006;
103(29):
11063 - 11068.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
A. Irintchev, A. Rollenhagen, E. Troncoso, J. Z. Kiss, and M. Schachner
Structural and Functional Aberrations in the Cerebral Cortex of Tenascin-C Deficient Mice
Cereb Cortex,
July 1, 2005;
15(7):
950 - 962.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. R. Evers, B. Salmen, O. Bukalo, A. Rollenhagen, M. R. Bosl, F. Morellini, U. Bartsch, A. Dityatev, and M. Schachner
Impairment of L-type Ca2+ Channel-Dependent Forms of Hippocampal Synaptic Plasticity in Mice Deficient in the Extracellular Matrix Glycoprotein Tenascin-C
J. Neurosci.,
August 15, 2002;
22(16):
7177 - 7194.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
D. D. S. Iglesia, P. H. Gala, T. Qiu, and M. A. Stepp
Integrin Expression During Epithelial Migration and Restratification in the Tenascin-C-deficient Mouse Cornea
J. Histochem. Cytochem.,
March 1, 2000;
48(3):
363 - 376.
[Abstract]
[Full Text]
|
|
|
|
|
|
|
J. Garwood, O. Schnadelbach, A. Clement, K. Schutte, A. Bach, and A. Faissner
DSD-1-Proteoglycan Is the Mouse Homolog of Phosphacan and Displays Opposing Effects on Neurite Outgrowth Dependent on Neuronal Lineage
J. Neurosci.,
May 15, 1999;
19(10):
3888 - 3899.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
E. Mackie and R. Tucker
The tenascin-C knockout revisited
J. Cell Sci.,
January 11, 1999;
112(22):
3847 - 3853.
[Abstract]
[PDF]
|
|
|
|
|
|
|
L. M. Moscoso, H. Cremer, and J. R. Sanes
Organization and Reorganization of Neuromuscular Junctions in Mice Lacking Neural Cell Adhesion Molecule, Tenascin-C, or Fibroblast Growth Factor-5
J. Neurosci.,
February 15, 1998;
18(4):
1465 - 1477.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. A. Stepp and L. Zhu
Upregulation of {alpha}9 Integrin and Tenascin During Epithelial Regeneration After Debridement in the Cornea
J. Histochem. Cytochem.,
February 1, 1997;
45(2):
189 - 202.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
