The present paper reports on the results obtained in a rabbit model of prenatal cocaine exposure that mimics the pharmacokinetics of crack cocaine in humans, and relates these findings to studies in other species including humans. A general finding is that prenatal exposure to cocaine during neurogenesis produces dysfunctions in signal transduction via the dopamine D(1) receptor and alterations in cortical neuronal development leading to permanent morphological abnormalities in frontocingulate cortex and other brain structures. Differences in the precise effects obtained appear to be due to the dose, route and time of cocaine administration. Related to these effects of in utero cocaine exposure, animals demonstrate permanent deficits in cognitive processes related to attentional focus that have been correlated with impairment of stimulus processing in the anterior cingulate cortex. The long-term cognitive deficits observed in various species are in agreement with recent reports indicating that persistent attentional and other cognitive deficits are evident in cocaine-exposed children as they grow older and are challenged to master more complex cognitive tasks.
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