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A Single Course of Prenatal Betamethasone in the Rat Alters Postnatal Brain Cell Proliferation but not Apoptosis
Author(s) -
Scheepens Arjan,
Waarenburg Marjo,
Hove Daniël,
Blanco Carlos E.
Publication year - 2003
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2003.043414
Subject(s) - betamethasone , endocrinology , apoptosis , bromodeoxyuridine , cell growth , medicine , corticosterone , neurogenesis , biology , neuroscience , hormone , immunohistochemistry , biochemistry
The aim of this study was to determine the effects of a clinically relevant single course of prenatal betamethasone in the rat on growth parameters with particular reference to brain cell proliferation and apoptosis. We report that administration of 170 μg kg −1 betamethasone twice within 4 h to E20 pregnant rats conveys moderate somatic growth retardation. Further, using a measure of brain cell proliferation independent of blood‐brain barrier (BBB) permeability, we demonstrate for the first time that betamethasone is chronically anti‐proliferative to brain cells without inducing caspase‐3‐mediated apoptosis. More importantly we show that there is a significant and sexually divergent rebound of neural proliferation which occurs earlier in males than in females and continues until at least 21 days of postnatal life. BBB permeability to [ 3 H]thymidine was significantly increased by steroid treatment re‐iterating the fact that tracer studies not correcting for BBB permeability, such as bromodeoxyuridine (BrdU), may be questionable in this type of study. Further, prenatal steroid treatment did not alter postnatal corticosterone levels. In summary we show that prenatal betamethasone conveys significant and long‐lasting side effects and that its human clinical application in preterm labour needs more careful consideration as compared to the relative ease with which it is prescribed today.