TY - JOUR
T1 - 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
AU - Antonow-Schlorke, Iwa
AU - Müller, Thomas
AU - Brodhun, Michael
AU - Wicher, Carola
AU - Schubert, Harald
AU - Nathanielsz, Peter W.
AU - Witte, Otto W.
AU - Schwab, Matthias
PY - 2007/6
Y1 - 2007/6
N2 - 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.
AB - 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.
KW - antenatal glucocorticoids
KW - brain
KW - fetal sheep
KW - neuronal cytoskeleton
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U2 - 10.1016/j.ajog.2006.10.898
DO - 10.1016/j.ajog.2006.10.898
M3 - Article
C2 - 17547892
AN - SCOPUS:34249748405
VL - 196
SP - 553.e1-553.e6
JO - American Journal of Obstetrics and Gynecology
JF - American Journal of Obstetrics and Gynecology
SN - 0002-9378
IS - 6
ER -