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Precise localization of glucose transport proteins in the brain has proved difficult, especially at the ultrastructural level. This has limited further insights into their cellular specificity, subcellular distribution, and function. In the present study, preembedding ultrastructural immunocytochemistry was used to localize the major brain glucose(More)
Leptin acts on specific brain regions to affect body weight regulation. As leptin is made by white adipose tissue, it is thought that leptin must cross the blood-brain barrier or the blood-cerebrospinal fluid barrier to reach key sites of action within the brain. High expression of a short form leptin receptor has been reported in the choroid plexus.(More)
Previous studies from our laboratory have demonstrated that chronic stress produces molecular, morphological, and ultrastructural changes in the rat hippocampus that are accompanied by cognitive deficits. Glucocorticoid attenuation of glucose utilization is proposed to be one of the causative factors involved in stress-induced changes in the hippocampus,(More)
The presence of GLUT4, the insulin-responsive glucose transporter, in microvascular endothelium and the responsiveness of glucose transport at the blood-brain barrier to insulin have been matters of controversy. To address these issues, we examined GLUT4 mRNA and protein expression in isolated brain microvessels and in cultured calf vascular cells derived(More)
The precise histologic localization of GLUT3, a glucose transporter thought to be restricted to neurons, is unknown. Using a high-affinity, specific antiserum against rodent GLUT3 for immunocytochemistry, light microscopic staining concentrates heterogeneously in the neuropil in a region- and lamina-specific manner; intense staining characterizes areas with(More)
Glucocorticoids induce hyperinsulinemia, hyperglycemia, and depress glucose transport by aortic endothelium. High glucocorticoid doses are used for many diseases, but with unknown effects on brain glucose transport or metabolism. This study tested the hypothesis that glucocorticoids affect glucose transport or metabolism by brain microvascular endothelium.(More)
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