Interestingly, they found that there was no change in overall production of D1 dopamine receptors in the brain, just their location in cells. Animal models can help determine how prenatal cocaine exposure might influence brain development to cause these subtle cognitive impairments. Studying the effects of prenatal cocaine exposure on the developing brain is difficult in human populations because cocaine abusers often abuse other drugs. However, the standard treatments for ADHD - Ritalin and other stimulants - are not always effective in these children. These children often exhibit attention and arousal problems, similar to children with attention deficit hyperactivity disorder ( ADHD ). "However, as those children age, they do develop deficits in their cognitive and emotional development." "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. 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. "The hysteria surrounding the 'crack baby' was sort of overblown," said Stanwood, research assistant professor of Pharmacology and lead author on the study.
Though this effect has not yet been assessed in cocaine-exposed children, the findings give researchers a place to start looking. Stanwood et al reported that prenatal cocaine exposure in pregnant rabbits caused a long-lasting disruption of D1 dopamine receptors. However the precise way that cocaine abuse disrupted proper cognitive development was unclear. Prenatal exposure to cocaine is known to cause a range of cognitive impairments ranging from attention deficits to severe emotional problems to mental retardation. 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. A recent study published in J.Neuroscience by Stanwood et al.
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