Past epidemiological studies suggest that germ cellssperm and eggsare more susceptible to reprogramming during the slow growth period of preadolescence.
Therefore, in this study, in order to examine the effects of paternal stress, male mice were exposed to six weeks of chronic stress, before breeding, either throughout puberty or only in adulthood. Examples of stress include sudden move to another cage, predator oder (fox urine, for example), noise, or a foreign object in the cage.
Male mice are ideal for such an experiment because they do not participate in offspring rearing, meaning any external factors outside of germ-cell formation are essentially eliminated.
Researchers found that offspring from paternal stress groups displayed significantly blunted levels of the stress hormone corticosteronein humans, it's cortisolin response to stress.
To understand the neural circuitry in the offspring, the group also examined changes in gene expression in certain brain regions involved in stress regulation: the paraventricular nucleus (PVN) and the bed nucleus of stria terminals.
They found an increased expression of glucocorticoid-responsive genes in the PVN, a change that supports a possible mechanism whereby increased negative feedback sensitivity may be explained.
The researchers also looked at a series of microRNAs (miRs) in the sperm that uniquely contribute to post-fertilization gene expression to examine the epigenetic mechanisms of transmission to the next generation. In both groups of stressed dads, there was a significant increase in expression of nine miRs. These miRs may be targeting the stored maternal messenger RNAs in the egg at fertilization, so that dad's sperm can regulate some aspect of early development to inform his offspring about the environment, according to the autho
|Contact: Steve Graff|
University of Pennsylvania School of Medicine