Title: Deconstructing Maternal Circuit Elements that Underlie Anxiety and Motivation
Need/Problem: Approximately 13-20% of perinatal women are afflicted by psychiatric illnesses, such as postpartum depression. These conditions impair maternal health, compromise mother-infant interactions, and have adverse implications for the developing offspring.
Grant Summary: Postpartum disorders may stem from perturbations in brain circuits that ordinarily act to promote maternal health and offspring care. However, a functional neural circuit level of understanding is poorly understood. For more effective treatments, it is necessary to gain a better understanding of the neural mechanisms that underlie both normal and pathological postpartum adaptations. The proposed research aims to establish a novel preclinical approach in a mouse model to elucidate the function of maternal circuit elements that affect infant care, anxiety, and motivation.
Goals & Projected Outcomes: The proposed research aims to establish a novel preclinical approach in a mouse model to elucidate the function of maternal circuit elements that affect infant care, anxiety, and motivation. The proposed experiments will likely advance our understanding of how the brain undergoes changes during the postpartum period, and how those alterations might affect anxiety, motivation, and mother-infant interactions. Additionally, these findings would provide strong preliminary data for multiple grant proposals to be submitted to NIH.
Grant Details: In the proposed experiments, we aim to permanently label neurons that are selectively engaged and recruited by the onset of maternal experience and establish whether direct re-activation or inhibition of these neurons alters reward and anxiety. Since maternal experience is considered to be a largely positive reinforced set of behaviors, we hypothesize that reactivation of these circuits will innately produce rewarding and anxiolytic phenotypes. In contrast, since maternal circuits are thought to facilitate maternal motivation and infant-induced anxiolysis, we predict that inhibition of maternally-responsive circuits will result in impaired maternal care, anxious and aversive phenotypes.