Meeting Abstract
The effects of maternal stress on offspring phenotype remain equivocal. An increase of circulating glucocorticoids in reproductive females may augment allocation of resources towards self-maintenance and away from offspring. Thus, elevated circulating glucocorticoids may negatively affect offspring development. However, maternal stress may induce preparative responses in offspring, such as higher tolerance to oxidative stress and more efficient mitochondria, which could positively impact survival. If early life experience is a good predictor of future environments, then increased mitochondrial performance may provide a benefit towards survival in poor conditions. To test this hypothesis, corticosterone (CORT) was administered orally to female mice from days 7 to 21 after parturition. Thus, offspring were indirectly exposed to CORT through the mother’s milk and aspects of their mitochondrial physiology were investigated at two timepoints, 38 and 70 days of age. At both ages, we isolated mitochondria from liver and skeletal muscle to measure respiratory control ratio (RCR) and reactive oxygen species (ROS) production. Preliminary results show that skeletal muscle RCR was higher while ROS was lower in adult offspring (70 days old) exposed to maternal CORT. These effects suggest potential benefits to post-natal stress exposure which could assist in predator escape. Experimental pups had a lower body mass than control pups at both ages, though these differences were marginally insignificant. Data on oxidative damage, mitochondrial density and fecal CORT levels will also be presented.
