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Effects of prenatal cocaine exposure on adolescent development.

ABSTRACT: The associations between prenatal cocaine exposure (PCE) and adolescent behavior, cognitive development, and physical growth were examined in 219 15-year-olds who have participated in a longitudinal study since their fourth gestational month. During the first trimester, 42% of the women used cocaine, with use declining across pregnancy. At the 15-year follow-up, the caregivers were, on average, 43 years old, had 13 years of education, and 50% were African American. First trimester PCE was not associated with global cognitive development or with measures of learning and memory. First trimester PCE was significantly related to adolescent-reported delinquent behavior, poorer problem solving and abstract reasoning, and reduced weight, height, and head circumference at 15 years. These results were significant after other factors that affect these domains were controlled in regression analyses. In addition, exposure to violence partially mediated the effect of PCE on delinquent behavior. These adolescent domains are important because they are predictors of poorer adult functioning.

SUBMITTER: Richardson GA

PROVIDER: S-EPMC4458454 | biostudies-literature | 2015 May-Jun

REPOSITORIES: biostudies-literature

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Effects of prenatal cocaine exposure on adolescent development.

Richardson Gale A GA Goldschmidt Lidush L Larkby Cynthia C Day Nancy L NL

Neurotoxicology and teratology 20150314

The associations between prenatal cocaine exposure (PCE) and adolescent behavior, cognitive development, and physical growth were examined in 219 15-year-olds who have participated in a longitudinal study since their fourth gestational month. During the first trimester, 42% of the women used cocaine, with use declining across pregnancy. At the 15-year follow-up, the caregivers were, on average, 43 years old, had 13 years of education, and 50% were African American. First trimester PCE was not as ...[more]

PMID: 25778776

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Project description:Prenatal cocaine exposure (PCE) can cause persistent neuropsychological and motor abnormalities in affected children, but the physiological consequences of PCE remain unclear. Conclusions drawn from clinical studies can sometimes be confounded by polysubstance abuse and nutritional deprivation. However, existing observations suggest that cocaine exposure in utero, as in adults, increases synaptic dopamine and promotes enduring dopamine-dependent plasticity at striatal synapses, altering behaviors and basal ganglia function.We used a combination of behavioral measures, electrophysiology, optical imaging, and biochemical and electrochemical recordings to examine corticostriatal activity in adolescent mice exposed to cocaine in utero.We show that PCE caused abnormal dopamine-dependent behaviors, including heightened excitation following stress and blunted locomotor augmentation after repeated treatment with amphetamine. These abnormal behaviors were consistent with abnormal ?-aminobutyric acid (GABA) interneuron function, which promoted a reversible depression in corticostriatal activity. PCE hyperpolarized and reduced tonic GABA currents in both fast-spiking and persistent low-threshold spiking type GABA interneurons to increase tonic inhibition at GABAB receptors on presynaptic corticostriatal terminals. Although D2 receptors paradoxically increased glutamate release following PCE, normal corticostriatal modulation by dopamine was reestablished with a GABAA receptor antagonist.The dynamic alterations at corticostriatal synapses that occur in response to PCE parallel the reported effects of repeated psychostimulants in mature animals, but differ in being specifically generated through GABAergic mechanisms. Our results indicate approaches that normalize GABA and D2 receptor-dependent synaptic plasticity may be useful for treating the behavioral effects of PCE and other developmental disorders that are generated through abnormal GABAergic signaling.

Project description:Prenatal cocaine exposure has been associated with numerous behavioral phenotypes in clinical populations, including impulsivity, reduced attention, alterations in social behaviors, and delayed language and sensory-motor development. Detecting associated changes in brain structure in these populations has proven difficult, and results have been inconclusive and inconsistent. Due to their more controlled designs, animal models may shed light on the neuroanatomical changes caused by prenatal cocaine; however, to maximize clinical relevance, data must be carefully collected using translational methods. The goal of this study was two-fold: (1) to determine if prenatal cocaine alters developmental neuroanatomy using methods that are available to human researchers, specifically structural MRI and diffusion tensor imaging, and (2) to determine the feasibility of rodent in vivo neuroimaging for usage in longitudinal studies of developmental disorders. Cocaine-exposed (prenatal days 1-20, 30mg/kg/day) rat pups were sedated and imaged live using diffusion tensor imaging and postmortem (fixed) using magnetic resonance histology on postnatal day 14. Volume and diffusion properties in whole brain as well as specific regions of interest were then assessed from the resulting images. Whole brain analyses revealed that cocaine-exposed animals showed no change in whole brain volume. Additionally, we found alterations in fractional anisotropy across regions associated with reward processing and emotional regulation, especially in the thalamus and globus pallidus, as well as sex-dependent effects of cocaine in the right cortex. Reductions in fractional anisotropy were paired with reductions only in axial diffusivity, which preliminarily suggests that the changes observed here may be due to axonal damage, as opposed to reductions in myelination of the affected regions/pathways. Our data indicate that prenatal cocaine may target a number of developing brain structures but does not result in overt changes to brain volumes. These results highlight not only the brain alterations that result from prenatal cocaine but also the advancements in live imaging that allow longitudinal study designs in other models.

Dataset Information

Effects of prenatal cocaine exposure on adolescent development.

Publications

Effects of prenatal cocaine exposure on adolescent development.

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