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Previous studies have found that stressful events during pregnancy can influence the developing fetus, resulting in attentional and neuromotor problems. This prospective study examined whether periods of vulnerability exist for neurobehavioral impairments associated with prenatal stress, using a nonhuman primate model. Twenty-eight rhesus monkey infants were born to mothers in 3 groups: (1) early gestation stress involving mild psychological stress from gestational days 45-90, (2) mid-late gestation stress from days 90-145, and (3) undisturbed controls. Infants were separated from their mothers on days 4, 9, 15, and 22 (+/- 1) postpartum for growth and neurobehavioral assessments. Results indicated that infants from the early gestation stress condition weighed less than infants from mothers stressed during mid-late gestation. Moreover, whereas both groups scored lower than controls on measures of attention and neuromotor maturity, early gestation stress was associated with more pronounced and more pervasive motor impairments than mid-late gestation stress. These results suggest sensitivity to prenatal stress effects peaks during early gestation, tapering off during mid-late gestation. Clarifying the period of greatest vulnerability to prenatal stress moves toward elucidating the underlying mechanism for prenatal stress effects and may lead to more successful intervention and/or prevention.

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The effect of stress to the pregnant mother on hormonal responses of the offspring to stressful events was investigated in juvenile rhesus monkeys. Six pregnant monkeys were repeatedly removed from their home cages and exposed to unpredictable noise during mid- to late gestation (Days 90-145 postconception), while six undisturbed pregnant mothers served as controls. Blood samples were collected from the juvenile offspring under anesthesia on four occasions and assayed for ACTH and cortisol. In a second experiment, blood samples were collected from the awake offspring under a baseline and four progressively stressful conditions. Offspring of stressed mothers showed higher ACTH and cortisol levels than control offspring at all four anesthesia samples and at a nonanesthesized home cage baseline. Prenatally stressed offspring also showed higher ACTH values in all four stress conditions. Cortisol values were similar for the two groups under the stress conditions. The disparity between the two groups in the relationship between ACTH and cortisol was greatest in the most stressful condition, suggesting regulatory differences between the two groups. These results indicate that offspring of primate mothers stressed during pregnancy show enhanced HPA axis responsivity to stressors later in life, and concur with rodent findings indicating that prenatal stress may have long-term effects on HPA axis regulation.

The use of alcohol by women during pregnancy is a continuing problem. In this review the behavioral effects of prenatal alcohol from animal models are described and related to studies of children and adults with FASD. Studies with monkeys and rodents show that prenatal alcohol exposure adversely affects neonatal orienting, attention and motor maturity, as well as activity level, executive function, response inhibition, and sensory processing later in life. The primate moderate dose behavioral findings fill an important gap between human correlational data and rodent mechanistic research. These animal findings are directly translatable to human findings. Moreover, primate studies that manipulated prenatal alcohol exposure and prenatal stress independently show that prenatal stress exacerbates prenatal alcohol-induced behavioral impairments, underscoring the need to consider stress-induced effects in fetal alcohol research. Studies in rodents and primates show long-term effects of prenatal and developmental alcohol exposure on dopamine system functioning, which could underpin the behavioral effects.