Date of Award




Document Type


Degree Name

Doctor of Philosophy (PhD)


Department of Psychology


Behavioral Neuroscience

Content Description

1 online resource (v, 181 pages) : illustrations (some color)

Dissertation/Thesis Chair

Joanna L Workman

Committee Members

Christine K Wagner, Damian G Zuloaga, Andrew M Poulos


dopamine, hippocampus, neurogenesis, Postpartum, prolactin, stress, Postpartum depression, Stress (Physiology), Hypothalamic-pituitary-adrenal axis, Breastfeeding, Rats as laboratory animals

Subject Categories

Biological Psychology | Neuroscience and Neurobiology | Psychology


Major depressive disorder is one of the most pervasive psychiatric illnesses in the United States. Women are at greater risk for developing depression, particularly during their childbearing years. Approximately 17% of new mothers develop postpartum depression within 4 weeks after parturition. The risk for postpartum depression is even greater in women who do not breastfeed or stop breastfeeding early. Major depressive disorder and postpartum depression share the same symptomology and common etiological bases. Dysregulated stress responses, dopamine activity, and neuroinflammation are recognized mechanisms for depression. The transition to motherhood encompasses physiological and behavioral adaptations in the brain essential for ensuring maternal care and offspring survival. Additionally, hypothalamus-pituitary-adrenal (HPA) axis activity is attenuated during the postpartum period. Neuroendocrine and neurobiological changes during the postpartum period may facilitate HPA axis hyporesponsivity through increased activation of brain structures that suppress HPA axis activity. The hippocampus is a key regulator of HPA axis activity and is sensitive to hormone action. Moreover, the hippocampus undergoes significant plasticity throughout the peripartum period. Perturbations in hippocampal neurogenesis and neural plasticity are implicated in a variety of psychiatric illnesses, including depression. Pleiotropic peptide hormone activity sustained through lactation may buffer against the development of depression during the postpartum period. Prolactin has multifaceted peripheral and central action both related and unrelated to lactation. Prolactin regulates aspects of neurogenesis, stress responses, dopaminergic activity, and neuroinflammatory responses, making it a strong candidate for contributing to stress resilience during the postpartum period. This dissertation aims to 1) delineate how reproductive state alters behavioral, endocrine, and neural stress responses in females, 2) investigate how experiential factors, like lactation and exposure to chronic stress, alter female stress responses in postpartum and nulliparous rats, and 3) identify potential neuroendocrine mechanisms for postpartum stress resilience. Together, these findings will better our understanding of how predisposing factors to psychiatric illnesses, like stress, affect female mammals at different reproductive states and have far-reaching implications for improving women’s healthcare and wellness across the lifespan.