Document Detail

Neurogenesis continues in the third trimester of pregnancy and is suppressed by premature birth.
MedLine Citation:
PMID:  23303921     Owner:  NLM     Status:  MEDLINE    
Premature infants exhibit neurodevelopmental delay and reduced growth of the cerebral cortex. However, the underlying mechanisms have remained elusive. Therefore, we hypothesized that neurogenesis in the ventricular and subventricular zones of the cerebral cortex would continue in the third trimester of pregnancy and that preterm birth would suppress neurogenesis. To test our hypotheses, we evaluated autopsy materials from human fetuses and preterm infants of 16-35 gestational weeks (gw). We noted that both cycling and noncycling Sox2(+) radial glial cells and Tbr2(+) intermediate progenitors were abundant in human preterm infants until 28 gw. However, their densities consistently decreased from 16 through 28 gw. To determine the effect of premature birth on neurogenesis, we used a rabbit model and compared preterm [embryonic day 29 (E29), 3 d old] and term (E32, <2 h old) pups at an equivalent postconceptional age. Glutamatergic neurogenesis was suppressed in preterm rabbits, as indicated by the reduced number of Tbr2(+) intermediate progenitors and the increased number of Sox2(+) radial glia. Additionally, hypoxia-inducible factor-1α, vascular endothelial growth factor, and erythropoietin were higher in term than preterm pups, reflecting the hypoxic intrauterine environment of just-born term pups. Proneural genes, including Pax6 and Neurogenin-1 and -2, were higher in preterm rabbit pups compared with term pups. Importantly, neurogenesis and associated factors were restored in preterm pups by treatment with dimethyloxallyl glycine, a hypoxia mimetic agent. Hence, glutamatergic neurogenesis continues in the premature infants, preterm birth suppresses neurogenesis, and hypoxia-mimetic agents might restore neurogenesis, enhance cortical growth, and improve neurodevelopmental outcome of premature infants.
Sabrina Malik; Govindaiah Vinukonda; Linnea R Vose; Daniel Diamond; Bala B R Bhimavarapu; Furong Hu; Muhammad T Zia; Robert Hevner; Nada Zecevic; Praveen Ballabh
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  The Journal of neuroscience : the official journal of the Society for Neuroscience     Volume:  33     ISSN:  1529-2401     ISO Abbreviation:  J. Neurosci.     Publication Date:  2013 Jan 
Date Detail:
Created Date:  2013-01-10     Completed Date:  2013-03-04     Revised Date:  2013-07-18    
Medline Journal Info:
Nlm Unique ID:  8102140     Medline TA:  J Neurosci     Country:  United States    
Other Details:
Languages:  eng     Pagination:  411-23     Citation Subset:  IM    
Department of Pediatrics, Regional Neonatal Center, Maria Fareri Children's Hospital at Westchester Medical Center and New York Medical College, Valhalla, New York 10595, USA.
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MeSH Terms
Anoxia / physiopathology
Cell Count
Cerebral Ventricles / growth & development
Erythropoietin / physiology
Gestational Age
Glycine / pharmacology
Hypoxia-Inducible Factor 1 / biosynthesis,  physiology
Infant, Newborn
Infant, Premature
Nerve Tissue Proteins / biosynthesis
Neural Stem Cells / physiology
Neurogenesis / physiology*
Pregnancy Trimester, Third / physiology*
Premature Birth / physiopathology*
Signal Transduction / physiology
Telencephalon / growth & development
Vascular Endothelial Growth Factor A / physiology
Wnt Proteins / physiology
beta Catenin / physiology
Grant Support
Reg. No./Substance:
0/Hypoxia-Inducible Factor 1; 0/Nerve Tissue Proteins; 0/Vascular Endothelial Growth Factor A; 0/Wnt Proteins; 0/beta Catenin; 11096-26-7/Erythropoietin; 56-40-6/Glycine

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

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