Lack of experience-mediated differences in the immunohistochemical expression of blood–brain barrier markers (EBA and GluT-1) during the postnatal development of the rat visual cortex

2005 ◽  
Vol 156 (2) ◽  
pp. 158-166 ◽  
Author(s):  
Enrike G. Argandoña ◽  
Harkaitz Bengoetxea ◽  
José V. Lafuente
Keyword(s):  
Visual Cortex ◽  
Postnatal Development ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Immunohistochemical Expression ◽  
Glut 1 ◽  
Blood Brain

GLUT-1 deficiency syndrome caused by haploinsufficiency of the blood-brain barrier hexose carrier

1998 ◽  
Vol 18 (2) ◽  
pp. 188-191 ◽  
Author(s):  
Glen Seidner ◽  
Marcela Garcia Alvarez ◽  
Jih-I Yeh ◽  
Kevin R. O'Driscoll ◽  
Jörg Klepper ◽  
...  
Keyword(s):  
Blood Brain Barrier ◽  
Deficiency Syndrome ◽  
Brain Barrier ◽  
Glut 1 ◽  
Blood Brain ◽  
Hexose Carrier

Subcellular distribution of glucose transporter (GLUT-1) during development of the blood-brain barrier in rats

1996 ◽  
Vol 284 (3) ◽  
pp. 355-365 ◽  
Author(s):  
Sylvia Bolz ◽  
Catherine L. Farrell ◽  
Klaus Dietz ◽  
Hartwig Wolburg
Keyword(s):  
Blood Brain Barrier ◽  
Subcellular Distribution ◽  
Glucose Transporter ◽  
Brain Barrier ◽  
Glut 1 ◽  
Blood Brain

Changes in the glucose transporter of brain capillaries

1992 ◽  
Vol 70 (S1) ◽  
pp. S113-S117 ◽  
Author(s):  
Sami I. Harik
Keyword(s):  
Alzheimer Disease ◽  
Blood Brain Barrier ◽  
Glucose Transporter ◽  
Glucose Transporters ◽  
Brain Barrier ◽  
Capillary Endothelium ◽  
Brain Capillaries ◽  
Glut 1 ◽  
Blood Brain ◽  
The Brain

Brain capillary endothelium has a high density of the GLUT-1 facilitative glucose transporter protein. This is reasonable in view of the brain's high metabolic rate for glucose and its isolation behind unique capillaries with blood – brain barrier properties. Thus, the brain endothelium, which constitutes less than 0.1% of the brain weight, has to transport glucose for the much larger mass of surrounding neurons and glia. I describe here the changes that occur in the density of glucose transporters in brain capillaries of subjects with Alzheimer disease, where there is a decreased cerebral metabolic rate for glucose, and in a novel clinical entity characterized by defective glucose transport at the blood – brain barrier. In subjects with Alzheimer disease, cerebral microvessels showed a marked decrease in the density of the glucose transporter when compared with age-matched controls, but there was no change in the density of glucose transporters in erythrocyte membranes. Thus, I believe that the decreased density of glucose transporters in the brains of subjects with Alzheimer disease is the result rather than the cause of the disease. In contradistinction, the primary defect in glucose transport at the blood – brain barrier in subjects with the recently described entity is associated with decreased density of GLUT-1 in erythrocyte membranes.Key words: brain microvessels, capillary endothelium, blood – brain barrier, glucose transporter, Alzheimer disease, hypoglycorrhachia.

17 beta-Estradiol modulation of glucose transporter 1 expression in blood-brain barrier

1997 ◽  
Vol 272 (6) ◽  
pp. E1016-E1022 ◽  
Author(s):  
J. Shi ◽  
J. W. Simpkins
Keyword(s):  
Endothelial Cells ◽  
Blood Brain Barrier ◽  
Glucose Transporter ◽  
Northern Blotting ◽  
Female Rats ◽  
Brain Barrier ◽  
Glucose Transporter 1 ◽  
Glut 1 ◽  
Blood Brain

The present study was designed to evaluate 17 beta-estradiol (E2) modulation of glucose transporter 1 (GLUT-1) protein and mRNA expression in blood-brain barrier (BBB) endothelium. Female rats were ovariectomized (OVX) for 12-14 days, then E2 was injected at dosages of 1-100 micrograms/kg sc at 2-16 h before sampling. Glucose transport into BBB endothelial cells was assessed using 2-deoxy-[14C]glucose (2-[14C]DG) uptake. GLUT-1 protein and mRNA samples were analyzed by Western and Northern blotting, respectively. E2 treatment caused dose- and time-dependent increases in 2-[14C]DG uptake and GLUT-1 protein expression by microvessels. The peak responses were induced by 10 micrograms/kg E2 dose at the 4-h sampling time (36.0 and 31.3% increases, P < 0.05, respectively). GLUT-1 mRNA demonstrated a transient increase at 15 min (55%, P < 0.05), then decreased to basal level by 2 h. This study shows that in vivo treatment with E2 increases 2-[14C]DG uptake into the BBB endothelial cells and suggests this E2 effect is due to its modulation of GLUT-1 mRNA and protein.

scholarly journals GLUT-1 glucose transporters in the blood-brain barrier: Differential phosphorylation

2011 ◽  
Vol 89 (12) ◽  
pp. 1913-1925 ◽  
Author(s):  
Kavi Devraj ◽  
Marianne E. Klinger ◽  
Roland L. Myers ◽  
Ashwini Mokashi ◽  
Richard A. Hawkins ◽  
...  
Keyword(s):  
Blood Brain Barrier ◽  
Glucose Transporters ◽  
Brain Barrier ◽  
Glut 1 ◽  
Blood Brain ◽  
Differential Phosphorylation
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