Document Detail


Growth defects in the dorsal pallium after genetically targeted ablation of principal preplate neurons and neuroblasts: a morphometric analysis.
MedLine Citation:
PMID:  20957077     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The present study delineates the large-scale, organic responses of growth in the dorsal pallium to targeted genetic ablations of the principal PP (preplate) neurons of the neocortex. Ganciclovir treatment during prenatal development [from E11 (embryonic age 11) to E13] of mice selectively killed cells with shared S-phase vulnerability and targeted expression of a GPT [golli promoter transgene; GPT linked to HSV-TK (herpes simplex virus-thymidine kinase), τ-eGFP and lacZ reporters] localized in PP neurons and their intermediate progenitor neuroblasts. The volume, area and thickness of the pallium were measured in an E12-P4 (postnatal age 4) longitudinal study with comparisons between ablated (HSV-TK(+/0)) and control (HSV-TK(0/0)) littermates. The extent of ablations was also systematically varied, and the effect on physical growth was assessed in an E18 cross-sectional study. The morphological evidence obtained in the present study supports the conclusion that genetically targeted ablations delay the settlement of the principal PP neurons of the dorsal pallium. This leads to progressive and substantial reductions of growth, despite compensatory responses that rapidly replace the ablated cells. These growth defects originate from inductive cellular interactions in the proliferative matrix of the ventricular zone of the pallium, but are amplified by subsequent morphogenic and trophic cellular interactions. The defects persist during the course of prenatal and postnatal development to demonstrate a constrained dose-response relationship with the extent of specific killing of GPT neurons. The defects propagate simultaneously in both the horizontal and vertical cytoarchitectural dimensions of the developing pallium, an outcome that produces a localized shortfall of volume in the telencephalic vesicles.
Authors:
Robin Fisher; Yuan-Yun Xie
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, N.I.H., Extramural     Date:  2010-10-04
Journal Detail:
Title:  ASN neuro     Volume:  2     ISSN:  1759-0914     ISO Abbreviation:  ASN Neuro     Publication Date:  2010  
Date Detail:
Created Date:  2010-10-19     Completed Date:  2011-12-08     Revised Date:  2013-07-03    
Medline Journal Info:
Nlm Unique ID:  101507115     Medline TA:  ASN Neuro     Country:  Unknown    
Other Details:
Languages:  eng     Pagination:  e00046     Citation Subset:  IM    
Affiliation:
Developmental and Molecular Neuroscience Group, Intellectual Development and Disabilities Research Center, Neuropsychiatric Institute, School of Medicine, The University of California at Los Angeles, Los Angeles, CA 90095, U.S.A. rfisher@mednet.ucla.edu
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MeSH Terms
Descriptor/Qualifier:
Animals
Animals, Newborn
Cross-Sectional Studies
Female
Gene Silencing*
Gene Targeting / methods*
Mice
Mice, Transgenic
Neural Stem Cells / pathology*,  physiology
Neurons / pathology*,  physiology
Pregnancy
Random Allocation
Telencephalon / abnormalities*,  pathology*,  physiology
Grant Support
ID/Acronym/Agency:
NS23022/NS/NINDS NIH HHS; NS33091/NS/NINDS NIH HHS
Comments/Corrections

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