Document Detail


Gene-chemical interactions in the developing mammalian nervous system: Effects on proliferation, neurogenesis and differentiation.
MedLine Citation:
PMID:  20381523     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The orderly formation of the nervous system requires a multitude of complex, integrated and simultaneously occurring processes. Neural progenitor cells expand through proliferation, commit to different cell fates, exit the cell cycle, generate different neuronal and glial cell types, and new neurons migrate to specified areas and establish synaptic connections. Gestational and perinatal exposure to environmental toxicants, pharmacological agents and drugs of abuse produce immediate, persistent or late-onset alterations in behavioral, cognitive, sensory and/or motor functions. These alterations reflect the disruption of the underlying processes of CNS formation and development. To determine the neurotoxic mechanisms that underlie these deficits it is necessary to analyze and dissect the complex molecular processes that occur during the proliferation, neurogenesis and differentiation of cells. This symposium will provide a framework for understanding the orchestrated events of neurogenesis, the coordination of proliferation and cell fate specification by selected genes, and the effects of well-known neurotoxicants on neurogenesis in the retina, hippocampus and cerebellum. These three tissues share common developmental profiles, mediate diverse neuronal activities and function, and thus provide important substrates for analysis. This paper summarizes four invited talks that were presented at the 12th International Neurotoxicology Association meeting held in Jerusalem, Israel during the summer of 2009. Donald A. Fox described the structural and functional alterations following low-level gestational lead exposure in children and rodents that produced a supernormal electroretinogram and selective increases in neurogenesis and cell proliferation of late-born retinal neurons (rod photoreceptors and bipolar cells), but not Müller glia cells, in mice. Lisa Opanashuk discussed how dioxin [TCDD] binding to the arylhydrocarbon receptor [AhR], a transcription factor that regulates xenobiotic metabolizing enzymes and growth factors, increased granule cell formation and apoptosis in the developing mouse cerebellum. Alex Zharkovsky described how postnatal early postnatal lead exposure decreased cell proliferation, neurogenesis and gene expression in the dentate gyrus of the adult hippocampus and its resultant behavioral effects. Bernard Weiss illustrated how environmental endocrine disruptors produced age- and sex-dependent alterations in synaptogenesis and cognitive behavior.
Authors:
Donald A Fox; Lisa Opanashuk; Aleksander Zharkovsky; Bernie Weiss
Related Documents :
10936193 - Glutamate receptor subunit delta2 is highly expressed in a novel population of glial-li...
19635473 - Shp2 acts downstream of sdf-1alpha/cxcr4 in guiding granule cell migration during cereb...
15126563 - Genistein enhances insulin-like growth factor signaling pathway in human breast cancer ...
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.     Date:  2010-04-08
Journal Detail:
Title:  Neurotoxicology     Volume:  31     ISSN:  1872-9711     ISO Abbreviation:  Neurotoxicology     Publication Date:  2010 Sep 
Date Detail:
Created Date:  2010-09-06     Completed Date:  2010-12-21     Revised Date:  2014-09-24    
Medline Journal Info:
Nlm Unique ID:  7905589     Medline TA:  Neurotoxicology     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  589-97     Citation Subset:  IM    
Copyright Information:
Copyright © 2010 Elsevier Inc. All rights reserved.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Animals
Cell Differentiation* / drug effects,  genetics
Cell Proliferation / drug effects*
Gene Expression Regulation, Developmental* / drug effects,  genetics
Humans
Mammals / genetics,  metabolism
Mice
Nervous System* / drug effects,  growth & development,  metabolism
Neurogenesis* / drug effects,  genetics
Neurotoxins / pharmacology*
Rats
Grant Support
ID/Acronym/Agency:
ES01247/ES/NIEHS NIH HHS; ES07026/ES/NIEHS NIH HHS; EY07551/EY/NEI NIH HHS; P30 ES001247-25S10108/ES/NIEHS NIH HHS; P30 EY007551/EY/NEI NIH HHS; P30 EY007551-24/EY/NEI NIH HHS; R01 ES012482-05/ES/NIEHS NIH HHS; R01 ES016357/ES/NIEHS NIH HHS; R01 ES016357-03/ES/NIEHS NIH HHS; R01ES012482/ES/NIEHS NIH HHS; R01ES015509/ES/NIEHS NIH HHS; R01ES016357/ES/NIEHS NIH HHS; R21ES013512/ES/NIEHS NIH HHS; T32 EY007024/EY/NEI NIH HHS; T32 EY007024-30/EY/NEI NIH HHS
Chemical
Reg. No./Substance:
0/Neurotoxins
Comments/Corrections

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


Previous Document:  What are the cognitive effects of stimulant medications? Emphasis on adults with attention-deficit/h...
Next Document:  Outbreaks of serious pneumococcal disease in closed settings in the post-antibiotic era: a systemati...