This research will investigate whether low-level ethanol and/or psychological stress exposure constitutes a danger to the developing fetus and what long-term effects emerge in and/or extend to adolescence. This question is difficult, if not impossible, to resolve in human studies. Our previous research, using a monkey model, has documented that prenatal stress and/or low-level ethanol exposure alter neonatal and infant development, as reflected by impaired neuromotor coordination, diminished attention span, and cognitive impairments. Evidence for enhanced stress reactivity in the juvenile stage suggests that problems also persist later in life. The proposed study will replicate and extend our nonhuman primate model of prenatal exposure to low-level ethanol and/or psychological stress during pregnancy.
Specific Aim 1 will be accomplished by examining the behavior and physiology of juvenile rhesus monkeys exposed in utero to ethanol, psychological stress, or ethanol and stress. We will monitor growth patterns, social and cognitive development and sires reactivity in these monkeys. Cognitive tests that identify damage to the hippocampal formation, a brain region particularly susceptible to prenatal ethanol and/or stress exposure will be used.
Specific Aim 2 will evaluate patterns of ethanol consumption in control and prenatally-exposed adolescent rhesus monkey offspring by examining physiologic responses to fixed quantities of ethanol as well as amount consumed using a voluntary 2-bottle choice paradigm.
Specific Aim 3 will involve the generation of an additional cohort of low-level ethanol exposed infants to determine the effects of gestational timing of exposure to ethanol. Because of the ability to ascertain timing and level of ethanol exposure during pregnancy, to separate the effects of ethanol from other life-style factors, and to explore possible mediating factors, these results will provide unique information on the long-term impact of early ethanol and/or stress exposure on offspring outcome.`
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