The long-term objective of this research is to elucidate the biosocial mechanisms involved in the etiology and impact of perinatal depression (PD) by linking early deficits in mother-infant coregulation to specific patterns of brain/neuroendocrine development that confer vulnerability to emotional dysregulation in the face of life stressors such as pregnancy and parenthood. These insights will be used to highlight women at risk for PD and to inform psychosocial and/or pharmacological treatment targets that block the transmission of depression risk. The immediate goal of this study is to test the hypothesis that PD mothers are distinguished by impaired emotion regulation in the context of their infant's distress at several interrelated levels of response: neural, neuroendocrine, and behavioral. To achieve this goal, I propose to 1) compare PD and non-PD mothers' patterns of neural response to their own infants' distress signals, 2) relate these patterns to mothers' hypothalamic-pituitary-adrenal (HPA) axis activity, and 3) relate these patterns to mothers' observed sensitivity to their infant. For this preliminary study, primiparous mothers who either show elevated depression across the perinatal period (PD group) or consistently low depression (non-PD group) are exposed to cry recordings and cry face images from their own and unfamiliar infants while undergoing functional neuroimaging. Contrasts between BOLD activity in different conditions (e.g., own vs. unfamiliar infant cry) will test response patterns within mothers/groups, as well as differences in response between PD and non-PD mothers. Mothers' salivary cortisol levels (indexing HPA activity) and behavioral sensitivity scores (both from a separate postnatal assessment) will also be entered as predictors of neural response to test brain-hormone-behavior associations in PD.
This research is important for public health because of the high cost of perinatal depression (PD), not only for the mother, but also for her infant's future development and mental health risk. However, the neurobiological basis for PD and its effects on the mother-infant dyad are not well understood. By identifying the patterns of neural response that distinguish perinatally depressed mothers and their relationship to aspects of behavioral and neuroendocrine dysregulation shown to harm the infant, we will be able to better characterize who is at risk and why, allowing for the development of more precise and efficacious treatment targets that will reduce the propagation of disorder. ? ? ?
