Effect of astroglial degeneration on neonatal blood-brain barrier marker expression.

Numerous studies have demonstrated that astroglial influence is necessary to maintain several blood-brain barrier (BBB) characteristics in CNS-derived endothelial cells in vitro. In the present study, we examined the hypothesis that intact perivascular astrocytes are essential contributors to the maintenance of particular BBB properties within the developing microvasculature of the postnatal rat CNS in situ. Astroglial cells were selectively injured following chronic systemic injections of the antimetabolite 6-aminonicotinamide (6-AN) during the first postnatal week. Throughout the CNS, the majority of perivascular astroglial endfeet were swollen and contained degenerating organelles. The brain microvasculature was examined at Postnatal Days 6-12 and the histochemical and immunohistochemical expressions of the brain endothelial glucose transporter (Glut1), gamma-glutamyltranspeptidase (gamma-GT), and endothelial barrier antigen (EBA) were qualitatively analyzed. Despite the apparent perivascular astroglial degeneration, all of the BBB markers examined were robustly expressed throughout the CNS and were comparable to age-matched controls. Moreover, 3[H]thymidine labeling revealed that the vascular endothelium continued to proliferate, albeit at a decreased rate when compared to age-matched controls. The results suggest that, in contrast to the majority of in vitro studies, the postnatal brain microvasculature continues to express Glut1, gamma-GT, and EBA in situ without the influence of continuously manufactured, astrocyte-derived substances.