Meeting Abstract
Exposure to stress during development can shape a broad range of phenotypic outcomes. In addition to programming response to stressors, these early experiences shape later life reproductive outcomes. Theoretical explorations of this phenomenon, drawing on life-history theory, suggest that both within-species and across-species variation in reproductive strategies would be predicted to be influenced by ecological factors indicative of resource availability and stressors (both physical and social). Endocrine, neurobiological and molecular studies suggest that the quality of the early environment – particularly qualities indicative of stress or threat – can have lasting effects on multiple biological systems. Epigenetic changes induced by these environmental exposures may mediate the link between stress and subsequent phenotypic outcomes. We have examined the epigenetic, neurobiological and behavioral consequences of early life stressors in rodents (rats and mice) with correlational studies also conducted in humans. Prenatal stress is associated with increased stress responsivity, altered neurodevelopmental trajectories and impairments in social and reproductive behaviors. These phenotypic outcomes are predicted by epigenetic variation in the placenta and associated with region-specific changes in gene expression and DNA methylation in the brain. Postnatal exposure to low vs. high stress environments is predictive of reduced maternal behavior and increased sexual behavior in later life. Altered DNA methylation of hormone sensitive genes in brain regions that regulate reproductive behavior may account for these effects. Future work on the trade-offs in phenotypic outcomes and the molecular mechanisms that shape these outcomes may provide further insights into the within and across-generation emergence of stress-induced reproductive strategies.
