title: Ontogeny of the erythroid/HepG2-type glucose transporter (GLUT-1) in the rat nervous system.
abstract: Central nervous system (CNS) microvessels of adult mammals have an unusually high density of the facilitative glucose transporter GLUT-1. Most systemic microvessels and those of the brain's circumventricular organs, which lack 'barrier' properties, do not express a high density of GLUT-1. Thus, a high GLUT-1 density is a marker of adult brain endothelium. To determine the stage at which CNS microvessels acquire GLUT-1, we studied by immunocytochemistry GLUT-1 ontogeny in the rat CNS from embryonic day (E) 11 to senescence. At E11, before blood vessels invaded the neuroectodermal tube, GLUT-1 immunoreactivity was already evident in the perineural plexus of vessels and in most of the vascular endothelium of the embryo. GLUT-1 immunoreactivity was also evident in the neuroectoderm. The neuroectoderm gradually lost GLUT-1 expression, and at about E16, GLUT-1 immunoreactivity was no longer detectable in most of the neuroectodermal epithelium, while CNS microvessels had increased their GLUT-1 immunoreactivity. By birth, GLUT-1 immunoreactivity in the CNS was restricted to the endothelium, the epithelium (but not the endothelium) of the choroid plexus, and tanycytes. This cellular distribution of GLUT-1 did not change much between birth and senescence despite considerable postnatal brain development and the increased brain capillary density. Our results suggest that while a CNS factor(s) may not have a role in the induction of the high expression of GLUT-1 in CNS endothelium, such a factor(s) is probably important in maintaining the high level of GLUT-1 in these endothelia.
authors.affiliation: Department of Neurology, Case Western Reserve University School of Medicine, Cleveland, OH.
authors.forename: S I
authors.initials: SI
authors.lastname: Harik
authors.forename: A K
authors.initials: AK
authors.lastname: Hall
authors.forename: P
authors.initials: P
authors.lastname: Richey
authors.forename: L
authors.initials: L
authors.lastname: Andersson
authors.forename: P
authors.initials: P
authors.lastname: Lundahl
authors.forename: G
authors.initials: G
authors.lastname: Perry
mesh_terms: D000375:Aging / Q000378:metabolism*; D000818:Animals; D001812:Blood-Brain Barrier; D001921:Brain / Q000196:embryology / Q000254:growth & development / Q000378:metabolism*; D002560:Cerebrovascular Circulation; D005314:Embryonic and Fetal Development / Q000502:physiology*; D004730:Endothelium, Vascular / Q000196:embryology / Q000254:growth & development / Q000378:metabolism; D004912:Erythrocytes / Q000378:metabolism; D005260:Female; D005333:Fetus / Q000166:cytology / Q000378:metabolism; D005865:Gestational Age; D006801:Humans; D007106:Immune Sera; D007150:Immunohistochemistry; D009004:Monosaccharide Transport Proteins / Q000032:analysis / Q000378:metabolism*; D011247:Pregnancy; D051381:Rats; D011916:Rats, Inbred F344; D017207:Rats, Sprague-Dawley; D014407:Tumor Cells, Cultured
chemical_list: D007106:Immune Sera; D009004:Monosaccharide Transport Proteins