TENASCIN KNOCKOUT MICE - BARRELS, BOUNDARY MOLECULES, AND GLIAL SCARS

In light of a previous report suggesting that the brains of tenascin-d eficient animals are grossly normal, we have studied the somatosensory cortical barrel field and injured cerebral cortex in postnatal homozy gous tenascin knockout, heterozygote, and normal wild-type mice. Nissl staining, cytochrome oxidase, and Dil axonal tracing of thalamocortic al axonal projections to the somatosensory cortex, all reveal the form ation of normal barrels in the first postnatal week in homozygous knoc kout mice that cannot be distinguished from heterozygote or normal wil d-type barrels. In addition to confirming the absence of tenascin in k nockout animals, and reporting apparently reduced levels of the glycop rotein in barrel boundaries of heterozygote animals using well-charact erized antibodies and immunocytochemistry, we also studied the DSD-1-P G proteoglycan, another developmentally regulated molecule known to be associated with transient glial/glycoconjugate boundaries that surrou nd developing barrels; DSD-1-PG was also found to be expressed in barr el boundaries in apparently normal time frames in tenascin knockout mi ce. Peanut agglutinin (PNA) binding of galactosyl-containing glycoconj ugates also revealed barrel boundaries in all three genotypes. We also examined the expression of tenascin-R, a paralog of tenascin-C (refer red to here simply as tenascin). As previously reported, tenascin-R is prominently expressed in subcortical white matter, and we found it wa s 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 distrib ution 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 reconside red in light of these findings on barrel development and cortical lesi ons in tenascin-deficient mice.