Effect of a single embryonic exposure to alcohol on glucose transporter (GLUT-1) distribution in brain vessels of aged mouse

Citation
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
Citations number
42
Categorie Soggetti
Neurosciences & Behavoir
Journal title
JOURNAL OF NEUROCYTOLOGY
ISSN journal
03004864 → ACNP
Volume
30
Issue
2
Year of publication
2001
Pages
167 - 174
Database
ISI
SICI code
0300-4864(200102)30:2<167:EOASEE>2.0.ZU;2-Q
Abstract
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.