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

• Published in: American journal of obstetrics and gynecology Vol. 196; no. 6; pp. 553.e1 - 553.e6
• Main Authors: Antonow-Schlorke, Iwa, MSc, Müller, Thomas, DVM, Brodhun, Michael, PhD, Wicher, Carola, PhD, Schubert, Harald, PhD, Nathanielsz, Peter W., MD, PhD, Witte, Otto W., MD, PhD, Schwab, Matthias, MD, PhD
• Format: Journal Article
• Language: English
• Published: United States Mosby, Inc 01.06.2007
• Subjects: Animals; antenatal glucocorticoids; Betamethasone - pharmacology; brain; Brain - metabolism; Brain - pathology; Dendrites - metabolism; Female; fetal sheep; Gestational Age; Glucocorticoids - pharmacology; Immunohistochemistry; Infusions, Intravenous; Microtubule-Associated Proteins - drug effects; Microtubule-Associated Proteins - metabolism; neuronal cytoskeleton; Neurons - metabolism; Obstetrics and Gynecology; Pregnancy; Sheep; antenatal glucocorticoids; brain; fetal sheep; neuronal cytoskeleton
• ISSN: 0002-9378; 1097-6868
• DOI: 10.1016/j.ajog.2006.10.898

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.