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Cocaine's Use During Pregnancy May Cause Lasting Cellular Effects

t 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.

A few years ago, Stanwood and Levitt, professor of Pharmacology and director of the Vanderbilt Kennedy Center, established such a model in rabbits. They found that exposure to low levels of intravenous cocaine during a very short window of time during gestation equivalent to the late first trimester and early second trimester in humans caused specific alterations in brain circuits that use the neurotransmitter dopamine.

Additionally, these cocaine-exposed offspring showed attention problems as well as insensitivity to stimulants like amphetamine, suggesting that cocaine exposure had altered the development of the dopamine pathways in the brain.

'In collaboration with Dr. Eitan Friedman of the City University of New York, we had previously shown a decrease in signaling of a particular receptor protein, the dopamine D1 receptor," Stanwood said. "We know that this receptor is involved in regulating the formation of cortical circuitry. It's also involved in the behavioral effects of amphetamines and cocaine.'

'The current study was an attempt to look at the mechanism of this decrease in D1 receptor signaling,' he said.

Stanwood examined the levels of D1 receptor in brain cells taken from 'teenage' rabbits that were exposed to cocaine during that short, sensitive prenatal period.

He found that cocaine exposure did not alter the total amount of D1 receptor produced in the brain. However, there was a dramatic alteration in the location of the protein within the cell.

'It's not where it should be,' he said. D1 receptors are normally found at the cell surface, but neurons from the cocaine-exposed animals showed the receptor was predominantly sequestered inside the
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