Previously, we analyzed the effects of prenatal cocaine exposure during the neocortical neuronogenesis (which in primates corresponds to the second trimester of gestation) on the development of the neocortex in rhesus monkeys. We found that the neocortex in such prenatally-cocaine-exposed monkeys is characterized by: (i) a loss of the normal lamination, (ii) an inappropriate positioning of the cortical neurons, and (iii) a reduction in the density and number of these neurons. We have also demonstrated that cocaine can induce these long-term effects only if it is administered during the period of neocortical neuronogenesis, with no such abnormalities being observed in the animals exposed to cocaine either prior to or after that developmental period. It is reasonable to hypothesize that these structural neocortical abnormalities in monkeys exposed to cocaine in utero are accompanied by behavioral deficits. The demonstration such deficits is important because it would not only validate the functional significance of the detected morphological changes, but also suggest which specific aspects of behavior may be compromised in children of drug-abusing human mothers. It is well documented that postnatal development of the primate brain is very prolonged with new functional capabilities appearing throughout neonatal, infant, juvenile and adolescent periods. The brain is also known for its remarkable adaptability. Consequently various behavioral deficits in our animals may not necessarily be continuously present throughout life; some of them may be detected only transiently as developmental retardations at certain stages of brain maturation, while others may appear later in life with maturation of their adult neural substrates. Therefore, an evaluation of behavior in prenatally cocaine-exposed animals should be done in a format of a longitudinal study. The goal of the present study is to employ longitudinal behavioral tests and observations to address the hypothesis that the significant prenatal cocaine-induced cerebral cortical structural disorganization is associated with identifiable behavioral deficits: I) We will determine whether neonatal monkeys in our model of prenatal cocaine exposure display deficits on items of the Neonatal Behavioral Assessment Scale; 2) We will assess whether infant, juvenile and adolescent monkeys with significant central cortical structural abnormalities, which are generated in our model of prenatal cocaine exposure, display deficits in specific cognitive, motor, and perceptual functions which rely on cerebral cortex as one of their major neural substrates; and 3) We will evaluate whether prenatal cocaine exposure producing cerebral cortical neuropathology in our animals affects normal development of non-social and social behaviors.
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