Day 2 has already been jam packed with lots of exciting findings presented here at Neuroscience 2013. In some weird, unintentional effort to wear myself out (what is wrong with me?) I’ve been going up and down the escalators, bouncing between the poster hall and talks all morning.
In one of my forays upstairs, I sat in on a short talk by Alice Graham from the University of Oregon. Graham presented a novel way to look at a commonly studied topic: early life stress. Citing a study that discovered obesity in individuals who experienced famine in utero as opposed to postnatally, Graham emphasized that there is a mismatch between pre- and postnatal environments when it comes to risk for disease. Instead of looking at stress at a specific time point in development (e.g. only prenatal), Graham proposed looking at the change in stress that occurs as an infant transitions from the pre- to postnatal environment.
This change in stress might be particularly evident in a variable such as interparental conflict. This variable, tested via response to an angry-toned voice, has been previously shown in Graham’s work to influence functional connectivity between the medial prefrontal cortex (mPFC) and other brain regions in infants. In a new study, Graham used self-report measures to show that interparental conflict is higher in the postnatal environment, meaning after a baby is born, as compared to the prenatal environment, meaning during pregnancy. Perhaps this has something to do with sleep deprivation and the screaming, spitting up bundle of joy, I’m not sure.
Since there is a difference in the stress due to interparental conflict that an infant might experience prenatally versus postnally, there may be differential effects of this stress on development. Graham studied this difference within the context of resting-state functional connectivity in the default mode network (DMN), a functional network in the brain that is active when someone is not specifically engaged in a task. Graham chose this network because it seems to be impacted by early life stress and it exhibits rapid development from 0 to 2 years of life.
When subtracting prenatal interparental conflict from postnatal interparental conflict, Graham showed that functional connectivity was increased between the posterior cingulate cortex and the following regions: mPFC, medial temporal lobe, inferior temporal gyrus, and the right amygdala. Thus, the postnatal increase in the stress an infant might experience due to interparental conflict seems to increase functional connectivity between several regions of the DMN, effectively speeding up the development of this network.
Perhaps this is an adaptive response to stress. However, Graham noted that another study has reported increased DMN functional connectivity in full term infants as compared to premature infants, meaning the less stressed, full term infants actually displayed greater DMN connectivity. This finding is in contrast to the findings of Graham’s group. Accordingly, further study of the effects of change in stress across development is necessary. Perhaps different types of stress have different effects at different times. As with most questions in neuroscience, this idea is compelling, yet extremely complicated.