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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.
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