Document Detail


Moderate alcohol exposure compromises neural tube midline development in prenatal brain.
MedLine Citation:
PMID:  12888216     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
We previously reported that fetal alcohol treatment compromised the development of the midline raphe and the serotonin neurons contained in it. In this study, we report that the timely development of midline neural tissue during neural tube formation is sensitive to alcohol exposure. Pregnant dams were treated from embryonic day 7 (E7, prior to neurulation) or E8.5 (at neurulation) with the following diets: (a) alcohol (ALC), given as either a 20% or 25% ethanol-derived calorie (EDC) liquid diet, or (b) isocaloric liquid diet pair-fed (PF), or (c) standard rat chow (Chow). Fetal brains from each group were examined on E13, E15, or E18. Neural tube development was compromised as a result of alcohol exposure in the following ways: (1) approximately 60% of embryos at E13 and 20% at E15 showed perforation of the floor plate in the diencephalic vesicle, (2) although completely closed at E13, 70-80% of embryos failed to complete the formation of neural tissue at the roof as the alcohol exposure continued to E15, and (3) 60-80% of embryos show delayed 'occlusion' of the ventral canal by newly formed nestin-positive neuroepithelial cells and S100beta-positive glia in the brainstem of E15. The compromised (incomplete) neural tube midline (cNTM) occurred near the ventricles at E13 and E15, but was later completed at E18. In all cases, the cNTM was accompanied by an enlarged ventricle, and dose-dependent brain weight reduction. The midline of the neural tube at the roof and floor plates is known to mediate timely trophic induction for neural differentiation. Prenatal midline deficits also have the potential to affect the development of midline neurons such as raphe, septal nuclei, and the timely crossing of commissural fibers. The results of the liquid diet alcohol exposure paradigm suggest it is more a model for Alcohol-Related Neurodevelopmental Disorder (ARND) featuring neuropsychiatric disorders than for full-blown fetal alcohol syndrome (FAS) with noticeable facial dysmorphogenesis and gross brain retardation.
Authors:
Feng C Zhou; Youssef Sari; Teresa Powrozek; Charles R Goodlett; Ting-Kai Li
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Publication Detail:
Type:  Comparative Study; In Vitro; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Brain research. Developmental brain research     Volume:  144     ISSN:  0165-3806     ISO Abbreviation:  Brain Res. Dev. Brain Res.     Publication Date:  2003 Aug 
Date Detail:
Created Date:  2003-07-30     Completed Date:  2003-10-03     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  8908639     Medline TA:  Brain Res Dev Brain Res     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  43-55     Citation Subset:  IM    
Affiliation:
Department of Anatomy and Cell Biology, Indiana University School of Medicine, 635 Barnhill Drive, Indianapolis, IN 46202, USA. imce100@iupui.edu
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MeSH Terms
Descriptor/Qualifier:
Animals
Body Patterning / drug effects
Brain / anatomy & histology,  drug effects*,  embryology,  metabolism
Central Nervous System Depressants / pharmacology*
Dose-Response Relationship, Drug
Ethanol / blood,  pharmacology*
Female
Food, Formulated
Growth Plate / drug effects,  embryology,  metabolism
Immunohistochemistry
Intermediate Filament Proteins / metabolism
Maternal Exposure
Mice
Mice, Inbred C57BL
Nerve Growth Factors / metabolism
Nerve Tissue Proteins*
Organ Size / drug effects
Pregnancy
Prenatal Exposure Delayed Effects
S100 Proteins / metabolism
Time Factors
Grant Support
ID/Acronym/Agency:
P50AA07611/P32/AA/NIAAA NIH HHS; R01AA12406/AA/NIAAA NIH HHS
Chemical
Reg. No./Substance:
0/Central Nervous System Depressants; 0/Intermediate Filament Proteins; 0/Nerve Growth Factors; 0/Nerve Tissue Proteins; 0/S-100 calcium-binding protein beta subunit; 0/S100 Proteins; 0/nestin; 64-17-5/Ethanol

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


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