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Journal of Child Neurology
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Transplacental Cocaine Exposure: A Mouse Model Demonstrating Neuroanatomic and Behavioral Abnormalities

Barry E. Kosofsky, MD, PhD

Laboratory of Molecular and Developmental Neuroscience Massachusetts General Hospital, Department of Neurology Massachusetts General Hospital and Harvard Medical School, Boston, MA

Aaron S. Wilkins, BS

Laboratory of Molecular and Developmental Neuroscience Massachusetts General Hospital

Pierre Gressens, MD

Laboratoire de Neurologie du Développement University of Louvain Medical School, Brussels, Belgium

Philippe Evrard, MD

Laboratoire de Neurologie du Développement University of Louvain Medical School, Brussels, Belgium

Between 10% and 15% of infants born in urban America today have been exposed to cocaine in utero. Clinical studies have suggested that impairment of brain growth is the single best marker of significant prenatal cocaine exposure, and postnatal developmental compromise seen in a subset of affected children as a consequence of that exposure. We have developed an animal model, in mice, of prenatal cocaine exposure that has allowed us to dissociate the direct effects of cocaine in altering fetal development from the indirect effects associated with cocaine-induced malnutrition. We find that transplacental cocaine exposure independently impairs fetal brain and body growth and results in behavioral deficits and permanent alterations in neocortical cytoarchitecture in exposed offspring. (J Child Neurol 1994;9:234-241).

Journal of Child Neurology, Vol. 9, No. 3, 234-241 (1994)
DOI: 10.1177/088307389400900303


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