Ontogenic expression of the erythroid-type glucose transporter (Glut 1) in the telencephalon of the mouse: correlation to the tightening of the blood-brain barrier.

Since Glut 1 was shown to be highly abundant in brain microvessels, its distribution during early developmental stages seems of importance in respect to the timing of blood-brain barrier (bbb) formation in the developing CNS. Here we have followed the temporal expression of the erythroid-type glucose transporter Glut 1 in the telencephalon of the embryonic and newborn mouse, beginning at the 9th intrauterine day. Glut 1 immunofluorescence staining was done on cryosections using a rabbit polyclonal antiserum to purified human erythrocyte glucose transporter. Endothelial cells resp. capillaries were detected by staining with a rhodamin-coupled Bandeiraea simplicifolia lectin (BSL). In parallel, the developmental tightening of the embryonic bbb was assessed by perfusion of mouse embryos with Trypan blue and horse radish-peroxidase. At E9, prior to the onset of intraneural neovascularization, strong Glut 1 immunoreactivity was found in the whole neuroectoderm but only minor staining was seen in the perineural domain. Glut 1 expression remained uniformly distributed in the intraneural tissue at E10, the beginning of intraneural neovascularization in the mouse. From E11 onwards, Glut 1 immunoreactivity was invisible in neuroepithelial cells, but appeared tightly associated with intraneural capillaries. Perfusion of E12 embryos using trypan blue solution and HRP revealed that most parts of the CNS and spinal cord were impermeable to the tracer substances at that stage. Thus, we suggest that the bbb is established very early in CNS development, probably in the course of intraneural neovascularization. In addition, our data indicate that the restriction of Glut 1 expression to the intraneural capillaries reflects the onset of bbb function in the mouse embryo.