A recent study by investigators at the Vanderbilt Kennedy Center for Research on Human Development may help explain the long-term behavioral and neurological problems associated with prenatal exposure to cocaine.
In a recent issue of the Journal of Neuroscience, Gregg Stanwood, Ph.D., and Pat Levitt, Ph.D., report that prenatal cocaine exposure in rabbits causes a long lasting displacement of dopamine receptors in certain brain cells, which alters their ability to function normally.
Though this effect has not yet been assessed in cocaine-exposed children, the findings give researchers a place to start looking.
“The hysteria surrounding the ‘crack baby’ was sort of overblown,” said Stanwood, research assistant professor of Pharmacology and lead author on the study.
Incredibly high levels of cocaine — usually coupled with the abuse of other drugs — can lead to premature labor, preterm birth and low birth weight, Stanwood said.
“But in women who have abused relatively low recreational doses of cocaine, it is actually very hard to distinguish those children at birth from children born to anyone else,” he said. “However, as those children age, they do develop deficits in their cognitive and emotional development.”
These children often exhibit attention and arousal problems, similar to children with attention deficit hyperactivity disorder (ADHD). However, the standard treatments for ADHD — Ritalin and other stimulants — are not always effective in these children.
Studying the effects of prenatal cocaine exposure on the developing brain is difficult in human populations because cocaine abusers often abuse other drugs. Animal models can help determine how prenatal cocaine exposure might influence brain development to cause these subtle cognitive impairments. “We thought that it was important to set up an animal model that recapitulates a key feature of human abuse — that being intravenous exposure to low doses of cocaine,” Stanwood said.