A growing literature indicates that prenatal exposure to cocaine exerts effects on the offspring that may be manifested as neurobehavioral deficits in children. In parallel, almost all of the current laboratory animal data are based on assessments conducted in neonatal or juvenile rodents. Few data are available to suggest the kinds of deficits that may appear during adulthood, and, especially, during advanced age. The latter period is especially important because, with aging, the reserve capacity of the brain may no longer be sufficient to compensate for damage inflicted during early brain development. Such an interaction is speculated to account for an accelerated onset of neurodegenerative disorders such as Parkinson's Disease. This question will be addressed in rats exposed during gestation, via maternal administration to cocaine. At 3-8, 9-14, 15-20, and 21-26 months of age, separate groups of rats will be assessed for latent damage by a variety of complex performance assays. These include measures of cognitive function (delayed choice), motor competence (running wheel performance), and drug discrimination capacity (ability to differentiate the effects of agents aimed at specific neurotransmitter systems). These measures will be supplemented by neurochemical assays, aimed at the dopamine system, designed to determine whether age-related variations in brain chemistry have been changed by the developmental exposure. These results will help estimate the full range of risks posed by maternal cocaine abuse and their potential impact on the community.
| Markowski, V P; Cox, C; Preston, R et al. (2000) Effects of age and gender but not prenatal cocaine on random ratio and delayed spatial alternation responding in rats. Neurotoxicol Teratol 22:421-8 |
| Weiss, B (1998) Neurobehavioral properties of chemical sensitivity syndromes. Neurotoxicology 19:259-68 |
| Weiss, B (1994) Low-level chemical sensitivity: a perspective from behavioral toxicology. Toxicol Ind Health 10:605-17 |
