The Neurobiological Etiology of Postpartum Depression: The Role of Oxytocin in the Hypothalamus and the Amygdala
Haverford College. Department of Psychology
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In the current study, we simulated the hormonal conditions of pregnancy and a postpartum period in a Syrian hamster model in order to better understand the neurobiological etiology of postpartum depression (PPD). PPD is a distinct subtype of major depressive disorder, which develops in new mothers during the first few weeks after delivery. It is a prevalent disorder and has incredibly harmful effects on both the mother and her infant, but not much is understood about its etiology, which makes treatment difficult. We hypothesized that after estrogen withdrawal produced a PPD-like state, subjects would show behavioral indicators of anhedonia through the Sucrose Preference Test. We also expected to find decreased levels of oxytocin producing cells in the paraventricular nucleus of the hypothalamus (PVN) and the medial amygdala of animals that experienced hormone withdrawal, which we believed might contribute to the development of PPD. We did not find any significant differences in the behavioral measures testing anhedonia. Our neurobiological findings were the opposite of what we hypothesized- we found significantly higher quantities of oxytocin producing neurons in the PVN of hamsters that experienced hormone withdrawal. These findings may indicate that oxytocin contributes to dysregulation of the HPA axis in the postpartum or that oxytocin fluctuations within the postpartum period affect PPD. Future research should further explore the role of oxytocin in the hypothalamus and amygdala, as it appears to be associated with PPD.