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Abstract

Distribution of glucose transporter (GLUT-1) in brain microvascular endothelium, representing the anatomic site of the blood-brain barrier (BBB), was studied with electron microscopy in 24-month-old mice, which had been exposed prenatally (on 9th day of gestation) to a single teratogenic dose of ethanol. Offspring of mice that had received an equivalent volume of isocaloric dextrose served as controls. Sections of brain samples embedded at low temperature in hydrophilic resin Lowicryl K4M were exposed to anti-GLUT-1 antiserum followed by gold-labelled secondary antibodies. By using morphometry, the labelling density was recorded over luminal and abluminal plasma membranes of the endothelial cells of blood microvessels supplying four brain regions: cortex, hippocampus, cerebellum and olfactory bulb. We found that the density of immunosignals for GLUT-1, represented by colloidal gold particles, was unchanged in the olfactory bulb and slightly lowered in the abluminal 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 immunolabelling 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 vasculature supplying different brain regions. In effect, the inefficient supply of glucose to selected brain regions can be one of the factors leading to the previously observed deficit in long-term memory in a similar alcohol-treated group of mice.

Targeting the β2-integrin LFA-1, reduces adverse neuroimmune actions in neuropathic susceptibility caused by prenatal alcohol exposure

“…It is possible that PAE the elevated basal expression of LFA-1 is a consequence of chronic aberrant ICAM-1 expression on vascular endothelial cells, which may be an underlying neuroimmune factor in the “primed” spinal cord of PAE rats leading to susceptibility upon a second challenge. In support of this possibility, a mouse model PAE lead to significantly lowered brain microvascular glucose transporter (GLUT-1) expression, a marker of functional brain microvessels [58]. BIRT-377 significantly decreases LFA-1 in PAE rats to levels similar to those measured from non-PAE Sac controls (Fig.…”

Cerebral Microvascular Density, Permeability of the Blood-Brain Barrier, and Neuroinflammatory Responses Indicate Early Aging Characteristics in a Marfan Syndrome Mouse Model

“…23,24 Aging is associated with a reduction in microvascular density, contributing to decreased cerebral blood flow, which can lead to impaired neurological function. 22,25,26 The MFS-associated premature aging phenotype and decreased cerebral blood flow velocity warrants further investigation to evaluate microvascular density in the brain.…”