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Intro: Working memory is the cognitive mechanism that enables us to temporarily hold information in our minds and manipulate it (Miyake et al., 2000). Working memory is essential to concentration, problem solving, many areas of learning, and is a prerequisite for long-term storage of information (Diamond, 2013; Hofmann, Schmeichal, & Baddeley, 2012). It is well-documented that children living in high-poverty have difficulties with working memory relative to their higher-income peers (Fry, Langley, & Shelton 2017). Human research provides evidence that poverty might influence the development of working memory via chronically elevated stress levels in early-life (Evans & Schamberg, 2009). Furthermore, poverty-related working memory difficulties have been associated with structural and functional differences in the prefrontal cortex (PFC) – a key brain region underlying working memory (Sheridan et al., 2012; Ursache & Noble, 2016). However, there is a paucity of research regarding neurobiological mechanisms by which poverty might account for difficulties in working memory. This is due to fundamental limitations that human researchers face in establishing causation to inform mechanisms through which poverty-related adversity influences development (Perry et al., 2018). In this cross-species study, we begin to translationally validate the use of a rodent model of scarcity-adversity to enable the study of neurobiological mechanisms by which poverty-related stress affects working memory.
Methods: Human data come from the Family Life Project, a population-based longitudinal sample (n=1292), which oversampled for impoverished families (Vernon-Feagans, et al., 2013). Using linear regression analyses, we assessed the association of early-life poverty-related risk (assessed at child ages 6-, 15-, and 24-months) with working memory skills when children were in 2nd grade while controlling for demographic factors. Rodent data come from a model of early-life scarcity-adversity. Using this rodent model, litters were randomly assigned into control conditions (mother was provided with ample materials for nest-building), or scarcity-adversity conditions (mother was provided with insufficient materials for nest-building) (Perry & Sullivan, 2014). After weaning, offspring were assessed in a test of working memory as peri-adolescents (spontaneous alternation; Lalonde, 2002). Glucocorticoid receptor expression in the PFC and hippocampus was quantified using Western blots to measure neural stress response activity.
Results: Linear regression analyses demonstrated a link between early-life poverty exposure and working memory impairments in Grade 2, even when controlling for an earlier measure of child executive function at 35 months (Figure 1). Rodent results revealed that early-life scarcity-adversity rearing resulted in working memory impairments in peri-adolescence (Figure 2), with evidence of upregulated glucocorticoid receptor levels in the PFC (p<0.05, n=8/group), but not the dorsal hippocampus (p=0.97, n=8/group).
Conclusion: Overall, human and rodent results indicate similarities in terms of early-life scarcity-adversity exposure and working memory skills in peri-adolescence. Furthermore, rodent results indicate that poverty-related adversity may influence working memory skills via altered glucocorticoid receptor expression in the PFC. Additional experiments using this rodent model will provide further insight into causal mechanisms by which poverty-related adversity disrupts the development of working memory.
Rosemarie E. Perry, New York University
Presenting Author
Stephen H. Braren, New York University
Non-Presenting Author
Annie Brandes-Aitken, Department of Applied Psychology, New York University
Non-Presenting Author
Cristina Alberini, New York University
Non-Presenting Author
Regina Sullivan, New York University School of Medicine
Non-Presenting Author
Clancy Blair, New York University
Non-Presenting Author