title: Alteration of rat fetal cerebral cortex development after prenatal exposure to polychlorinated biphenyls.
abstract: Polychlorinated biphenyls (PCBs) are environmental contaminants that persist in environment and human tissues. Perinatal exposure to these endocrine disruptors causes cognitive deficits and learning disabilities in children. These effects may involve their ability to interfere with thyroid hormone (TH) action. We tested the hypothesis that developmental exposure to PCBs can concomitantly alter TH levels and TH-regulated events during cerebral cortex development: progenitor proliferation, cell cycle exit and neuron migration. Pregnant rats exposed to the commercial PCB mixture Aroclor 1254 ended gestation with reduced total and free serum thyroxine levels. Exposure to Aroclor 1254 increased cell cycle exit of the neuronal progenitors and delayed radial neuronal migration in the fetal cortex. Progenitor cell proliferation, cell death and differentiation rate were not altered by prenatal exposure to PCBs. Given that PCBs remain ubiquitous, though diminishing, contaminants in human systems, it is important that we further understand their deleterious effects in the brain.
authors.affiliation: Developmental Neuroendocrinology unit, GIGA Neurosciences, University of Liège, CHU, Liège, Belgium.
authors.forename: Elise
authors.initials: E
authors.lastname: Naveau
authors.affiliation: Developmental Neuroendocrinology unit, GIGA Neurosciences, University of Liège, CHU, Liège, Belgium.
authors.forename: Anneline
authors.initials: A
authors.lastname: Pinson
authors.affiliation: Developmental Neuroendocrinology unit, GIGA Neurosciences, University of Liège, CHU, Liège, Belgium.
authors.forename: Arlette
authors.initials: A
authors.lastname: Gérard
authors.affiliation: Developmental Neurobiology unit, GIGA Neurosciences, University of Liège, CHU, Liège, Belgium.
authors.forename: Laurent
authors.initials: L
authors.lastname: Nguyen
authors.affiliation: Laboratory of Clinical, Forensic and Environmental Toxicology, University of Liège, CHU, Liège, Belgium.
authors.forename: Corinne
authors.initials: C
authors.lastname: Charlier
authors.affiliation: Laboratory of Animal Ecology and Ecotoxicology (LEAE, CART), University of Liège, Liège, Belgium.
authors.forename: Jean-Pierre
authors.initials: JP
authors.lastname: Thomé
authors.affiliation: Biology Department, University of Massachusetts, Morrill Science Center, Amherst, Massachusetts, United States of America.
authors.forename: R Thomas
authors.initials: RT
authors.lastname: Zoeller
authors.affiliation: Developmental Neuroendocrinology unit, GIGA Neurosciences, University of Liège, CHU, Liège, Belgium.
authors.forename: Jean-Pierre
authors.initials: JP
authors.lastname: Bourguignon
authors.affiliation: Developmental Neuroendocrinology unit, GIGA Neurosciences, University of Liège, CHU, Liège, Belgium.
authors.forename: Anne-Simone
authors.initials: AS
authors.lastname: Parent
mesh_terms: D000818:Animals; D002453:Cell Cycle / Q000187:drug effects; D016923:Cell Death; D002454:Cell Differentiation; D002465:Cell Movement; D049109:Cell Proliferation; D002540:Cerebral Cortex / Q000187:drug effects* / Q000254:growth & development / Q000473:pathology; D020111:Chlorodiphenyl (54% Chlorine) / Q000494:pharmacology*; D015536:Down-Regulation; D052244:Endocrine Disruptors / Q000494:pharmacology*; D004785:Environmental Pollutants / Q000494:pharmacology*; D005260:Female; D005333:Fetus; D058953:Neural Stem Cells / Q000166:cytology / Q000187:drug effects; D009474:Neurons / Q000187:drug effects* / Q000473:pathology; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000097:blood* / Q000473:pathology / Q000503:physiopathology; D051381:Rats; D013974:Thyroxine / Q000097:blood
chemical_list: D052244:Endocrine Disruptors; D004785:Environmental Pollutants; D020111:Chlorodiphenyl (54% Chlorine); D013974:Thyroxine