Pattern of glucose transporter (Glut 1) expression in embryonic brains is related to maturation of blood-brain barrier tightness.

A constant supply of blood-borne glucose is vital to cerebral metabolism. Although transport of glucose into the nervous tissue, effectively separated from the blood by a functional barrier (the blood-brain barrier, BBB), is one of the essential properties of the cerebral endothelium, little is known about its metabolic regulation and developmental expression in the BBB. In this study we provide evidence by immunocytochemistry that the pattern of the brain endothelial glucose transporter in rat brains (BBB-GT), immunologically homologous with the human hepatoma (G2), human erythrocyte transporter (Glut 1), changes with BBB maturation. While the neuroepithelium at embryonic days 12 and 13 shows a high incidence of immuno-detectable BBB-GT, vascularisation of the cerebral anlage and subsequent development of vascular tightness, as evidenced by intravascularly applied horseradish peroxidase and fluorescinated dextrans, is accompanied by a significant reduction of BBB-GT expression in neuroepithelial cells and confinement of BBB-GT expression to the cerebral endothelium. Immunoblots and Northern blots of embryonic brain homogenates corroborate this change in BBB-GT expression in the brain anlage at the time of BBB maturation. However, low molecular weight glucose transporters, presumed to be of non-endothelial origin, are less dramatically reduced. The development of BBB tightness, therefore, seems to play a pivotal role in the pattern of BBB-GT expression during brain differentiation.