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Effect of Antenatal Dexamethasone Treatment on Neuronal Morphogenesis.
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HOME > J Pathol Transl Med > Volume 39(2); 2005 > Article
Original Article Effect of Antenatal Dexamethasone Treatment on Neuronal Morphogenesis.
Soo Jeong Yoon, Heasoo Koo, Chong Il Kim
Journal of Pathology and Translational Medicine 2005;39(2):81-90
DOI: https://doi.org/
1Department of Pathology, Ewha Womans University, College of Medicine, Seoul, Korea. heasoo@ewha.ac.kr
2Department of Obstetrics and Gynecology, Ewha Womans University, College of Medicine, Seoul, Korea.
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BACKGROUND
Glucocorticoids (GCs) are essential for normal development and the maturation of the central nervous system. The aim of this study was to determine the effects of antenatal dexamethasone (DEXA) treatment on neuronal morphogenesis and on the glial cell line-derived neurotrophic factor (GDNF) protein expression in neonatal rat.
METHODS
Pregnant Sprague-Dawley rats were injected with saline (the control), or 0.2 mg/kg/day DEXA or 0.8 mg/kg/day DEXA at 17th, 18th and 19th day of gestation. The newborn rat brains were examined at postnatal days 1 (n=75) and 10 (n=78).
RESULTS
The DEXA-treated groups showed distorted architectures of neurons in the cerebral cortex, hippocampus and cerebellar cortex at postnatal days 1 and 10 with an increased number of proliferating cell nuclear antigen (PCNA)-positive cells. The cerebellar cortex in the DEXA-treated groups showed delayed development with more PCNA-positive cells in the internal granular cell layer. The Purkinje cells showed a markedly decreased number and the decreased length of the dendritic processes. The GDNF positive reaction was decreased in the DEXA-treated groups in a dose-dependent manner.
CONCLUSIONS
The developmental changes and neuronal degeneration at postnatal days 1 and 10 in the newborn rats that were exposed to DEXA at the late gestational age were associated with increased proliferative activity and a decreased level of GDNF protein expression.

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