A recent study published in J.Neuroscience by Stanwood et al. may help explain the long-term neurological effects associated with cocaine use while pregnant, the so-called “crack baby syndrome” which was of great concern in the 1980s. Prenatal exposure to cocaine is known to cause a range of cognitive impairments ranging from attention deficits to severe emotional problems to mental retardation. However the precise way that cocaine abuse disrupted proper cognitive development was unclear.
Stanwood et al reported that prenatal cocaine exposure in pregnant rabbits caused a long-lasting disruption of D1 dopamine receptors.
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.
Interestingly, they found that there was no change in overall production of D1 dopamine receptors in the brain, just their location in cells. Usually D1s are found at the cell’s surface, but the neurons of cocaine-exposed animals have significantly less at the cells’ surface. They are much more likely to be inactive, inside the cell. And, it seems as though these changes are permanent and irreversible, suggesting that developmental exposure to cocaine results in very significant lifetime effects.