Document Detail


Stress in pregnancy activates neurosteroid production in the fetal brain.
MedLine Citation:
PMID:  17164539     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Neurosteroids such as allopregnanolone are potent agonists at the GABA(A) receptor and suppress the fetal CNS activity. These steroids are synthesized in the fetal brain either from cholesterol or from circulating precursors derived from the placenta. The concentrations of allopregnanolone are remarkably high in the fetal brain and rise further in response to acute hypoxic stress, induced by constriction of the umbilical cord. This response may result from the increased 5alpha-reductase and cytochrome P-450(SCC) expression in the brain. These observations suggest that the rise in neurosteroid concentrations in response to acute hypoxia may represent an endogenous protective mechanism that reduces excitotoxicity following hypoxic stress in the developing brain. In contrast to acute stress, chronic hypoxemia induces neurosteroidogenic enzyme expression without an increase in neurosteroid concentrations and, therefore, may pose a greater risk to the fetus. At birth, the allopregnanolone concentrations in the brain fall markedly, probably due to the loss of placental precursors; however, stressors, including hypoxia and endotoxin-induced inflammation, raise allopregnanolone concentrations in the newborn brain. This may protect the newborn brain from hypoxia-induced damage. However, the rise in allopregnanolone concentrations was also associated with increased sleep. This rise in sedative steroid levels may depress arousal and contribute to the risk of sudden infant death syndrome. Our recent findings indicate that acute hypoxic stress in pregnancy initiates a neurosteroid response that may protect the fetal brain from hypoxia-induced cell death, whereas the decline in allopregnanolone levels after birth may result in greater vulnerability to brain injury in neonates.
Authors:
Jonathan J Hirst; Tamara Yawno; Phuong Nguyen; David W Walker
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Review     Date:  2006-12-11
Journal Detail:
Title:  Neuroendocrinology     Volume:  84     ISSN:  0028-3835     ISO Abbreviation:  Neuroendocrinology     Publication Date:  2006  
Date Detail:
Created Date:  2007-03-05     Completed Date:  2007-05-01     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0035665     Medline TA:  Neuroendocrinology     Country:  Switzerland    
Other Details:
Languages:  eng     Pagination:  264-74     Citation Subset:  IM    
Copyright Information:
Copyright (c) 2006 S. Karger AG, Basel.
Affiliation:
School of Biomedical Sciences, University of Newcastle, Callaghan, Australia. Jon.Hirst@newcastle.edu.au
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MeSH Terms
Descriptor/Qualifier:
Animals
Asphyxia / metabolism
Brain / embryology,  metabolism*
Female
Fetus / metabolism*
Hypoxia, Brain / metabolism
Pregnancy
Pregnanolone / metabolism*
Prenatal Injuries / metabolism
Receptors, GABA-A / metabolism
Stress, Psychological / metabolism*
Chemical
Reg. No./Substance:
0/Receptors, GABA-A; 128-20-1/Pregnanolone

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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