We have investigated the expression of tenascin-C (TN-C) in the somatosensory cortex of early postnatal mutant mice in which lacZ was reported to be expressed in place of tenascin (Saga et al.: Genes Dev 6:1821-1831, 1992). At both the mRNA and protein levels, TN-C was detected at levels lower in the mutant than in wild type animals by in situ hybridization and by immunocytochemistry using several poly- and monoclonal antibodies directed against mouse TN-C. The distribution of TN-C immunoreactivity in coronal sections was abnormal in that the barrel field boundaries in layer 4 of the somatosensory cortex could not be detected intracellularly in most cell bodies, including possibly also neurons. Western blot analysis of homogenates of brain tissue from early postnatal animals showed an abnormal pattern of protein bands immunoreactive for TN-C in mutant animals while beta-galactosidase migrated at its expected molecular weight without incorporation into fusion proteins with TN-C, suggesting disturbed splicing mechanisms. No gross disturbances in the patterning of barrel fields could be detected in the mutant mice as shown by Nissl staining. Our observations show that the mutant mouse designed to be nully disrupted for TN-C expression shows detectable and abnormal TN-C expression.