Infancy is an extended developmental process during which an enormous amount of information is incorporated into the brain. Thus, if the brain's capacity for experience-dependent growth and modification were degraded even slightly by low level exposures to Superfund chemicals, cognitive performance might be impaired for a lifetime. We hypothesize that brain plasticity emerging late in development will be a very sensitive biomarker for detecting subtle damage suffered by brain cells during earlier stages of brain development. To test this, we will employ a model using extensively to document the key role of experience in organizing behavioral abilities and synaptic circuits in young animals. We predict that rats exposed during pre- and early postnatal neural development to Superfund toxicants will show deficits in brain plasticity after weaning in lower doses than they would show defects in brain morphogenesis. Because this approach tests a broad functional endpoint of development, it is appropriate for real world mixtures of Superfund chemicals. If the experiments confirm diminished behaviorally-induced gene expression as a biomarker of threshold neurotoxic defects, this novel model would provide a rapid and efficient means of screening the mature nervous system for developmental damage.

Agency
National Institute of Health (NIH)
Institute
National Institute of Environmental Health Sciences (NIEHS)
Type
Hazardous Substances Basic Research Grants Program (NIEHS) (P42)
Project #
5P42ES010338-02
Application #
6443979
Study Section
Special Emphasis Panel (ZES1)
Project Start
2001-04-01
Project End
2002-03-31
Budget Start
Budget End
Support Year
2
Fiscal Year
2001
Total Cost
$100,818
Indirect Cost
Name
Oregon Health and Science University
Department
Type
DUNS #
009584210
City
Portland
State
OR
Country
United States
Zip Code
97239
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