Glucose transporter proteins GLUT1 and GLUT3 like immunoreactivities in the fetal sheep brain are not reduced by maternal betamethasone treatment

Iwa Antonow-Schlorke, Martin Ebert, Thomas Müller, Harald Schubert, Andrea Gschanes, Otto W. Witte, Peter W. Nathanielsz, Matthias Schwab

Research output: Contribution to journalArticlepeer-review

2 Scopus citations

Abstract

Synthetic glucocorticoids administered to accelerate fetal lung maturation in threatened preterm delivery change electrocortical brain activity in the human and sheep fetus and alter structural neuronal proteins in fetal baboon and sheep. We hypothesized that these changes are due to a decreased amount of glucose transporter proteins (GLUT). Glucose uptake into cerebral neurons is selectively facilitated by glucose transporter protein GLUT1 in the blood brain barrier and GLUT3 in neuronal membranes. GLUT1 and GLUT3 immunoreactivity was examined in fetal sheep brain sections of the frontal neocortex, caudate putamen and hippocampus at 0.73 gestation after fetal exposure to betamethasone by direct fetal intravenous infusion or maternal intramuscular injections at the clinically relevant dosage. Betamethasone did not alter GLUT1 and GLUT3 immunoreactivity in any of the brain regions investigated, independently of the dose and route of administration. These data indicate that alteration of GLUT expression is unlikely to explain the cerebral functional effects of antenatal glucocorticoids.

Original languageEnglish (US)
Pages (from-to)261-265
Number of pages5
JournalNeuroscience Letters
Volume403
Issue number3
DOIs
StatePublished - Aug 7 2006

Keywords

  • Antenatal glucocorticoids
  • Brain glucose transporter proteins
  • Fetus
  • Immunohistochemistry
  • Sheep

ASJC Scopus subject areas

  • Neuroscience(all)

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