Transplacental cocaine exposure: a mouse model demonstrating neuroanatomic and behavioral abnormalities.
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.
Kosofsky
B E
BE
Laboratory of Molecular and Developmental Neuroscience, Massachusetts General Hospital, Charlestown 02129.
Wilkins
A S
AS
Gressens
P
P
Evrard
P
P
D000014:Abnormalities, Drug-Induced / Q000209:etiology*; D000818:Animals; D000831:Animals, Newborn / Q000254:growth & development; D001921:Brain / Q000187:drug effects; D001927:Brain Diseases / Q000139:chemically induced; D003042:Cocaine / Q000009:adverse effects* / Q000494:pharmacology; D004195:Disease Models, Animal; D005314:Embryonic and Fetal Development / Q000187:drug effects*; D005260:Female; D006130:Growth Disorders / Q000139:chemically induced; D008431:Maternal-Fetal Exchange; D051379:Mice / Q000254:growth & development*; D009474:Neurons / Q000187:drug effects; D011247:Pregnancy
D003042:Cocaine