I have studied the temporal and spatial regulation of the expression of the extracellular matrix protein tenascin in the developing chick brain using immunological and in situ hybridization methods. Tenascin is barely detectable by immuno‐slot blot analysis in the E4 telencephalon, but increases rapidly in abundance until E14, when the level of expression tapers off. The late appearance of tenascin was confirmed by immunohistochemistry. Tenascin can not be detected at E4, but at E7 is distributed homogeneously in most parts of the central nervous system. Tenascin is much less abundant in the retina than in other brain areas. As the avian retina is devoid of both vasculature and fibronectin, this supports the notion that tenascin may mask fibronectin from migrating growth cones and cell bodies. I have also used in situ hybridization with a cDNA probe to determine the origins of tenascin in the developing nervous system. Tenascin transcript is found in regions of glial proliferation and the cell bodies of radial glia. In contrast, tenascin appears to be made by neurons in the retina. As a low‐molecular weight splice variant of tenascin is detected on western blots of retina homogenates, different cell types may be responsible for generating the multiple forms of tenascin found in whole brain homogenates.
ASJC Scopus subject areas
- Animal Science and Zoology