Aw. Vorbrodt et al., Effect of a single embryonic exposure to alcohol on glucose transporter (GLUT-1) distribution in brain vessels of aged mouse, J NEUROCYT, 30(2), 2001, pp. 167-174
Distribution of glucose transporter (GLUT-1) in brain microvascular endothe
lium, representing the anatomic site of the blood-brain barrier (BBB), was
studied with electron microscopy in 24-month-old mice, which had been expos
ed prenatally (on 9th day of gestation) to a single teratogenic dose of eth
anol. Offspring of mice that had received an equivalent volume of isocalori
c dextrose served as controls. Sections of brain samples embedded at low te
mperature in hydrophilic resin Lowicryl K4M were exposed to anti-GLUT-1 ant
iserum followed by gold-labelled secondary antibodies. By using morphometry
, the labelling density was recorded over luminal and abluminal plasma memb
ranes of the endothelial cells of blood microvessels supplying four brain r
egions: cortex, hippocampus, cerebellum and olfactory bulb. We found that t
he density of immunosignals for GLUT-1, represented by colloidal gold parti
cles, was unchanged in the olfactory bulb and slightly lowered in the ablum
inal plasmalemma of the vascular endothelium in the cerebral cortex of the
ethanol-treated mice. In contrast, statistical analysis using Mann-Whitney
U-test revealed that in the hippocampus and cerebellum, the density of immu
nolabelling of both plasma membranes of microvascular endothelial cells was
significantly lowered in the ethanol-treated mice. These findings suggest
that prenatally applied ethanol had a different influence on the vasculatur
e supplying different brain regions. In effect, the inefficient supply of g
lucose to selected brain regions can be one of the factors leading to the p
reviously observed deficit in long-term memory in a similar alcohol-treated
group of mice.