Immunohistochemical detectability of cerebrovascular utrophin depends on the condition of basal lamina

Abstract Utrophin is an autosomal homologue of dystrophin. Dystrophin is a member of the dystrophin–glycoprotein complex, which is a cell surface receptor for basal lamina components. In recent opinions utrophin occurs in the cerebrovascular endothelium but not in the perivascular glia. Cerebrovascular laminin immunoreactivity can only be detected in the subpial segments of the vessels, in circumventricular organs lacking blood–brain barrier, in immature vessels and following brain lesions. In our former experience utrophin immunoreactivity showed similar phenomena to that of laminin. The present study investigates the parallel occurrence of vascular utrophin and laminin immunoreactivity in the brain tissue, especially in the circumventricular organs, and during the parallel postnatal regression of both utrophin and laminin immunoreactivity. Their cerebrovascular immunoreactivity observed in frozen sections renders plausible the role of hidden but explorable epitopes, instead of a real absence of laminin and utrophin. The laminin epitopes are supposed to be hidden due to the fusion of the glial (i.e. brain parenchymal) and vascular basal laminae (Krum et al., Exp. Neurol. 111 (1991) 151). In all cases including its post-lesion re-appearance published formerly by us, laminin immunoreactivity may be attributed to the separation of glial and vascular basal laminae. Utrophin is localized, however, intracellularly, therefore a more complex molecular mechanism is to be assumed and it remains to be investigated how structural changes of the basal lamina may indirectly affect the immunoreactivity of utrophin. The results indicate that immunoreactivity may be influenced not only by the presence or absence of macromolecules but also by their functional state.