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Abstract

The distribution of glucose transporter (GLUT-1) and of interendothelial junction-associated proteins--zonula occludens protein (ZO-1), occludin, and beta-catenin--was studied using quantitative immunogold procedure. Lowicryl K4M-embedded samples of the cerebral cortex of 1-, 7-, and 14-day-, and 6-week-old (young-adult) mice were used. Ultrathin sections were exposed to specific rabbit polyclonal antibodies followed by colloidal gold-labelled secondary antibodies. We found that the density of immunosignals for GLUT-1 in both luminal and abluminal plasma membranes of the endothelial cells, and those closely related to the interendothelial junctions was low in blood microvessels from newborn mice, dropped slightly at the 7th day, and increased through the 14th day to the level of mature blood-brain barrier (BBB) observed in 6-week-old mice. The expression of ZO-1 was high in newborn mice and increased at the 7th day to the level similar to that found in 14-day- and 6-week-old mice. The expression of occludin was less intense than that of ZO-1 and increased from birth, reaching at the 14th day the level typical for mature BBB found in young-adult animals. The immunosignals for occludin were sparsely distributed inside the junctional clefts. Such a distribution indicates that the tight junctional characteristics are limited to a few short segments of the entire interendothelial cleft. The density of immunosignals for beta-catenin was lowest, and it had the tendency to a gradual, although inconsiderable, drop in the time course of BBB maturation. These findings suggest that the relatively high concentration of GLUT-1 in the interendothelial junctions results from the participation of abluminal plasma membranes of adjacent endothelial cells in the formation of the junctional complexes. The interendothelial junctions of newborn mice are equipped already with the main components of the tight junctions, and the concentration of these components (ZO-1, occludin) reaches the level of the mature BBB at the 14th day of postnatal life.

Suppression of brain cholesterol synthesis in male Mecp2-deficient mice is age dependent and not accompanied by a concurrent change in the rate of fatty acid synthesis

“…3), and earlier (Buchovecky et al, 2013), show that the fall in brain cholesterol synthesis in the mutants is not seen in organs like the liver and lung. Taken together then, all these findings point to a selective suppression in cholesterol synthesis in the developing brain starting at about the time that closure of the blood brain barrier is purported to occur in the mouse (Vorbrodt et al, 2001). …”

Development of the blood–brain barrier within the paraventricular nucleus of the hypothalamus: influence of fetal glucocorticoid excess

“…Differences in leakage among circumventricular organs were shown using FITC even though all are fenestrated and lack a BBB (Morita and Miyata 2012 ). Many BBB studies predominantly focus on the cortex for changes (e.g., Sadowska et al 2009 ; Daneman et al 2010 ; Vorbrodt et al 2001 ; Ezan et al 2012 ; Armulik et al 2010 ; Bell et al 2010 ) and occasionally examine the cerebellum (Sadowska et al 2009 ; Armulik et al 2010 ). For BBB development, reports indicate cortical leakage of high molecular weight dyes until postnatal day 21 in rats (Utsumi et al 2000 ), and postnatal day 14 in mice (Lossinsky et al 1986 ; Vorbrodt et al 1986 ).…”

Glial Glucokinase Expression in Adult and Post-Natal Development of the Hypothalamic Region

“…This suggests that GK functional activity is increased when the blood–brain barrier reaches the mature level with the weaning (Vorbrodt et al, 2001). In the second week, GK was broadly distributed in the cytoplasm of the tanycytes but not in the nucleus.…”