Previous work with various animal models has demonstrated that alterations in the caregiving environment produce long-term changes in anxiety-related and social behaviors, as well as amygdala gene expression. We previously introduced a rodent model in which the timing and duration of exposure to maltreatment or nurturing care outside the home cage can be controlled to assess neurobiological outcomes. Here we sought to determine whether our brief experimental conditions produce changes in gene expression within the developing and adult amygdala. Using a candidate gene approach, we examined fold mRNA changes for the Brain-derived neurotrophic factor (Bdnf), Oxytocin receptor (OXTr), and Neuropeptide Y (NPY) genes, which are all highly expressed in the amygdala and play important roles in anxiety-related and social behaviors. In adults, significant group differences were detected for only Bdnf, with higher levels of Bdnf mRNA for females that had been exposed to maltreatment and males exposed to nurturing care outside the home cage relative to littermate controls. For pups, significant group differences were detected for only OXTr, with lower levels of OXTr mRNA in females exposed to maltreatment. Finally, for adolescents, maltreated-females showed significant changes in Bdnf (decreased), OXTr (decreased), and NPY (increased) mRNA relative to controls. These data illustrate the ability of brief, but repeated exposure to different caregiving environments during the first postnatal week to have long-term effects on gene expression within the developing and adult amygdala, especially for females.
Within the past decade we have experienced a paradigm shift in our understanding of gene–environment interactions and pathways through which experiences can become part of our biology. Advances in molecular biology have provided new insights into epigenetic factors (e.g., DNA methylation, histone acetylation) that are remarkably sensitive to environmental input and capable of registering and perpetuating altered gene activity states without affecting the underlying sequence of DNA. Groundbreaking studies have revealed that environmental adversity, social stress, and traumatic experiences can become encoded within epigenetic factors that control gene activity. As will be highlighted here, the birth of epigenetics research has provided an exciting new level of analysis for understanding tenets central to the discipline of developmental psychopathology, and a candidate biological pathway linking gene–environment interactions to long‐term and even multigenerational trajectories in the development of behavior.
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