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

Abstract

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. Fetal sheep received 3.3 microg 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). 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. Alteration of neuronal cytoskeletal proteins caused by antenatal betamethasone exposure is transient and independent of age during late gestation.