Betamethasone-related acute alterations of microtubule-associated proteins in the fetal sheep brain are reversible and independent of age during the last one-third of gestation

Iwa Antonow-Schlorke, Thomas Müller, Michael Brodhun, Carola Wicher, Harald Schubert, Peter W. Nathanielsz, Otto W. Witte, Matthias Schwab

Research output: Contribution to journalArticlepeer-review

8 Scopus citations

Abstract

Objective: The purpose of this study was to examine whether glucocorticoid effects on neuronal cytoskeleton, which we have shown previously at 0.87 gestation when the hypothalamo-pituitary-adrenal axis matures, are age-dependent and reversible. Study Design: Fetal sheep received 3.3 μg kg-1 h-1 betamethasone (n = 10) or saline solution (n = 9) intravenously over 48 hours at 0.75 gestation (ie, before the hypothalamo-pituitary-adrenal axis matures and when betamethasone is administered clinically). Results: Betamethasone diminished microtubule-associated protein (MAP) 1B and 2 immunoreactivity in the frontal neocortex and caudate putamen (P < .05) and MAP2 in the hippocampus (P < .05), which is similar to the effects that are seen at 0.87 gestation. In agreement, the number of glucocorticoid receptors did not differ at both ages. Loss of MAP1B and MAP2 immunoreactivity was not accompanied by neuronal death and was reversible within 24 hours. Conclusion: Alteration of neuronal cytoskeletal proteins caused by antenatal betamethasone exposure is transient and independent of age during late gestation.

Original languageEnglish (US)
Pages (from-to)553.e1-553.e6
JournalAmerican Journal of Obstetrics and Gynecology
Volume196
Issue number6
DOIs
StatePublished - Jun 2007
Externally publishedYes

Keywords

  • antenatal glucocorticoids
  • brain
  • fetal sheep
  • neuronal cytoskeleton

ASJC Scopus subject areas

  • Obstetrics and Gynecology

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